PMID- 34051305
OWN - NLM
STAT- Publisher
LR  - 20210529
IS  - 1873-4847 (Electronic)
IS  - 0955-2863 (Linking)
DP  - 2021 May 26
TI  - The synergistic protection of EGCG and quercetin against streptozotocin 
      (STZ)-induced NIT-1 pancreatic β cell damage via upregulation of BCL-2 expression by 
      miR-16-5p.
PG  - 108748
LID - S0955-2863(21)00168-6 [pii]
LID - 10.1016/j.jnutbio.2021.108748 [doi]
AB  - EGCG and quercetin are flavonoids which usually co-exist in edible plants and they 
      exhibit anti-diabetes effects. This study aimed to explore the mechanisms by which 
      quercetin and EGCG synergistically protected pancreatic β-cells from 
      streptozotocin-induced apoptosis. EGCG, quercetin, and their combinations (both 15 
      μM) all reversed STZ-induced cells damage and enhanced glucose-stimulated insulin 
      secretion, with the combination being more effective than a single compound. At the 
      molecular level, the EGCG-quercetin combination upregulated BCL-2 expression and 
      caused a greater reduction in miR-16-5p level than EGCG alone or quercetin alone. 
      Overexpression of miR-16-5p could offset the down-regulated apoptotic genes caused 
      by the synergistic action of the combination. These findings suggest that EGCG and 
      quercetin exert synergistic anti-diabetes effect, possibly via decreasing the 
      expression of miR-16-5p that targets directly BCL-2. This is the first report on a 
      miRNA-based mechanism underlying the synergistic protective effect of EGCG and 
      quercetin against pancreatic cell damage.
CI  - Copyright © 2021 Elsevier Ltd. All rights reserved.
FAU - Liu, Hui
AU  - Liu H
AD  - College of Food Science and Engineering, Shandong Agricultural University, Key 
      Laboratory of Food Processing Technology and Quality Control of Shandong Higher 
      Education Institutes, Taian 271018, P.R. China.
FAU - Wang, Lu
AU  - Wang L
AD  - College of Food Science and Engineering, Shandong Agricultural University, Key 
      Laboratory of Food Processing Technology and Quality Control of Shandong Higher 
      Education Institutes, Taian 271018, P.R. China.
FAU - Li, Feng
AU  - Li F
AD  - College of Food Science and Engineering, Shandong Agricultural University, Key 
      Laboratory of Food Processing Technology and Quality Control of Shandong Higher 
      Education Institutes, Taian 271018, P.R. China.
FAU - Jiang, Yang
AU  - Jiang Y
AD  - College of Food Science and Engineering, Shandong Agricultural University, Key 
      Laboratory of Food Processing Technology and Quality Control of Shandong Higher 
      Education Institutes, Taian 271018, P.R. China.
FAU - Guan, Hui
AU  - Guan H
AD  - College of Food Science and Engineering, Shandong Agricultural University, Key 
      Laboratory of Food Processing Technology and Quality Control of Shandong Higher 
      Education Institutes, Taian 271018, P.R. China.
FAU - Wang, Dan
AU  - Wang D
AD  - College of Food Science and Engineering, Shandong Agricultural University, Key 
      Laboratory of Food Processing Technology and Quality Control of Shandong Higher 
      Education Institutes, Taian 271018, P.R. China.
FAU - Sun-Waterhouse, Dongxiao
AU  - Sun-Waterhouse D
AD  - College of Food Science and Engineering, Shandong Agricultural University, Key 
      Laboratory of Food Processing Technology and Quality Control of Shandong Higher 
      Education Institutes, Taian 271018, P.R. China; School of Chemical Sciences, The 
      University of Auckland, New Zealand.
FAU - Wu, Maoyu
AU  - Wu M
AD  - Jinan fruit research institute of all-china supply and marketing cooperatives, 
      Jinan, 250014, China.
FAU - Li, Dapeng
AU  - Li D
AD  - College of Food Science and Engineering, Shandong Agricultural University, Key 
      Laboratory of Food Processing Technology and Quality Control of Shandong Higher 
      Education Institutes, Taian 271018, P.R. China. Electronic address: 
      dpli73@sdau.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20210526
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
SB  - IM
OTO - NOTNLM
OT  - BCL-2
OT  - EGCG
OT  - diabetes
OT  - miR-16-5p
OT  - quercetin
OT  - synergism
EDAT- 2021/05/30 06:00
MHDA- 2021/05/30 06:00
CRDT- 2021/05/29 20:10
PHST- 2020/05/25 00:00 [received]
PHST- 2020/12/15 00:00 [revised]
PHST- 2021/03/30 00:00 [accepted]
PHST- 2021/05/29 20:10 [entrez]
PHST- 2021/05/30 06:00 [pubmed]
PHST- 2021/05/30 06:00 [medline]
AID - S0955-2863(21)00168-6 [pii]
AID - 10.1016/j.jnutbio.2021.108748 [doi]
PST - aheadofprint
SO  - J Nutr Biochem. 2021 May 26:108748. doi: 10.1016/j.jnutbio.2021.108748.

PMID- 34038674
OWN - NLM
STAT- Publisher
LR  - 20210526
IS  - 1547-6898 (Electronic)
IS  - 1040-8444 (Linking)
DP  - 2021 May 26
TI  - Methodological considerations for measuring biofluid-based microRNA biomarkers.
PG  - 1-37
LID - 10.1080/10408444.2021.1907530 [doi]
AB  - MicroRNAs (miRNAs) are small non-coding RNA that regulate the expression of 
      messenger RNA and are implicated in almost all cellular processes. Importantly, 
      miRNAs can be released extracellularly and are stable in these matrices where they 
      may serve as indicators of organ or cell-specific toxicity, disease, and biological 
      status. There has thus been great enthusiasm for developing miRNAs as biomarkers of 
      adverse outcomes for scientific, regulatory, and clinical purposes. Despite advances 
      in measurement capabilities for miRNAs, miRNAs are still not routinely employed as 
      noninvasive biomarkers. This is in part due to the lack of standard approaches for 
      sample preparation and miRNA measurement and uncertainty in their biological 
      interpretation. Members of the microRNA Biomarkers Workgroup within the Health and 
      Environmental Sciences Institute's (HESI) Committee on Emerging Systems Toxicology 
      for the Assessment of Risk (eSTAR) are a consortium of private- and public-sector 
      scientists dedicated to developing miRNAs as applied biomarkers. Here, we explore 
      major impediments to routine acceptance and use of miRNA biomarkers and case 
      examples of successes and deficiencies in development. Finally, we provide insight 
      on miRNA measurement, collection, and analysis tools to provide solid footing for 
      addressing knowledge gaps toward routine biomarker use.
FAU - Chorley, Brian N
AU  - Chorley BN
AUID- ORCID: 0000-0002-0676-1383
AD  - U.S. Environmental Protection Agency, Research Triangle Park, NC, USA.
FAU - Atabakhsh, Elnaz
AU  - Atabakhsh E
AD  - Abcam Inc., Cambridge, MA, USA.
FAU - Doran, Graeme
AU  - Doran G
AD  - Abcam Inc., Cambridge, MA, USA.
FAU - Gautier, Jean-Charles
AU  - Gautier JC
AD  - Sanofi R&D, Vitry-sur-Seine, France.
FAU - Ellinger-Ziegelbauer, Heidrun
AU  - Ellinger-Ziegelbauer H
AD  - Department of Pharmaceuticals, Bayer AG, Wuppertal, Germany.
FAU - Jackson, David
AU  - Jackson D
AUID- ORCID: 0000-0001-9263-6011
AD  - Walter Reed Army Institute of Research, Silver Spring, MD, USA.
FAU - Sharapova, Tatiana
AU  - Sharapova T
AD  - AbbVie, North Chicago, IL, USA.
FAU - Yuen, Peter S T
AU  - Yuen PST
AD  - National Institute of Diabetes and Digestive and Kidney Diseases, National 
      Institutes of Health, Bethesda, MD, USA.
FAU - Church, Rachel J
AU  - Church RJ
AD  - Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, NC, USA.
FAU - Couttet, Philippe
AU  - Couttet P
AD  - Novartis Pharma AG, Basel, Switzerland.
FAU - Froetschl, Roland
AU  - Froetschl R
AD  - Federal Institute for Drugs and Medical Devices, Bonn, Germany.
FAU - McDuffie, James
AU  - McDuffie J
AD  - Janssen Research & Development, LLC, San Diego, CA, USA.
FAU - Martinez, Victor
AU  - Martinez V
AD  - BC Cancer Research Centre, Vancouver, BC, Canada.
FAU - Pande, Parimal
AU  - Pande P
AD  - Boehringer Ingelheim, Ridgefield, CT, USA.
FAU - Peel, Lauren
AU  - Peel L
AD  - Health and Environmental Sciences Institute, Washington, DC, USA.
FAU - Rafferty, Conor
AU  - Rafferty C
AD  - Abcam Inc., Cambridge, MA, USA.
FAU - Simutis, Frank J
AU  - Simutis FJ
AD  - Bristol-Myers Squibb Company, New Brunswick, NJ, USA.
FAU - Harrill, Alison H
AU  - Harrill AH
AD  - National Institute of Environmental Health Sciences, Research Triangle Park, NC, 
      USA.
LA  - eng
PT  - Journal Article
DEP - 20210526
PL  - England
TA  - Crit Rev Toxicol
JT  - Critical reviews in toxicology
JID - 8914275
SB  - IM
OTO - NOTNLM
OT  - MicroRNAs
OT  - biofluids
OT  - biomarkers
OT  - clinical
OT  - qualification
OT  - regulation
OT  - review
OT  - safety assessment
EDAT- 2021/05/27 06:00
MHDA- 2021/05/27 06:00
CRDT- 2021/05/26 20:09
PHST- 2021/05/26 20:09 [entrez]
PHST- 2021/05/27 06:00 [pubmed]
PHST- 2021/05/27 06:00 [medline]
AID - 10.1080/10408444.2021.1907530 [doi]
PST - aheadofprint
SO  - Crit Rev Toxicol. 2021 May 26:1-37. doi: 10.1080/10408444.2021.1907530.

PMID- 34033143
OWN - NLM
STAT- In-Data-Review
LR  - 20210525
IS  - 1530-6860 (Electronic)
IS  - 0892-6638 (Linking)
VI  - 35
IP  - 6
DP  - 2021 Jun
TI  - Mechanical overload-induced muscle-derived extracellular vesicles promote adipose 
      tissue lipolysis.
PG  - e21644
LID - 10.1096/fj.202100242R [doi]
AB  - How regular physical activity is able to improve health remains poorly understood. 
      The release of factors from skeletal muscle following exercise has been proposed as 
      a possible mechanism mediating such systemic benefits. We describe a mechanism 
      wherein skeletal muscle, in response to a hypertrophic stimulus induced by 
      mechanical overload (MOV), released extracellular vesicles (EVs) containing 
      muscle-specific miR-1 that were preferentially taken up by epidydimal white adipose 
      tissue (eWAT). In eWAT, miR-1 promoted adrenergic signaling and lipolysis by 
      targeting Tfap2α, a known repressor of Adrβ3 expression. Inhibiting EV release 
      prevented the MOV-induced increase in eWAT miR-1 abundance and expression of 
      lipolytic genes. Resistance exercise decreased skeletal muscle miR-1 expression with 
      a concomitant increase in plasma EV miR-1 abundance, suggesting a similar mechanism 
      may be operative in humans. Altogether, these findings demonstrate that skeletal 
      muscle promotes metabolic adaptations in adipose tissue in response to MOV via 
      EV-mediated delivery of miR-1.
CI  - © 2021 Federation of American Societies for Experimental Biology.
FAU - Vechetti, Ivan J Jr
AU  - Vechetti IJ Jr
AUID- ORCID: 0000-0003-1024-1011
AD  - Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, 
      Lincoln, NE, USA.
AD  - Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
FAU - Peck, Bailey D
AU  - Peck BD
AD  - Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
AD  - Department of Physical Therapy, University of Kentucky, Lexington, KY, USA.
FAU - Wen, Yuan
AU  - Wen Y
AD  - Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, 
      Lincoln, NE, USA.
AD  - Department of Physical Therapy, University of Kentucky, Lexington, KY, USA.
FAU - Walton, R Grace
AU  - Walton RG
AD  - Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
AD  - Department of Physical Therapy, University of Kentucky, Lexington, KY, USA.
FAU - Valentino, Taylor R
AU  - Valentino TR
AD  - Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
AD  - Department of Physiology, University of Kentucky, Lexington, KY, USA.
FAU - Alimov, Alexander P
AU  - Alimov AP
AD  - Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
AD  - Department of Physiology, University of Kentucky, Lexington, KY, USA.
FAU - Dungan, Cory M
AU  - Dungan CM
AD  - Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
AD  - Department of Physical Therapy, University of Kentucky, Lexington, KY, USA.
FAU - Van Pelt, Douglas W
AU  - Van Pelt DW
AD  - Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
AD  - Department of Physical Therapy, University of Kentucky, Lexington, KY, USA.
FAU - von Walden, Ferdinand
AU  - von Walden F
AD  - Division of Neuropediatrics, Department of Women's and Children's Health, Karolinska 
      Institutet, Solna, Sweden.
FAU - Alkner, Björn
AU  - Alkner B
AD  - Division of Neuropediatrics, Department of Women's and Children's Health, Karolinska 
      Institutet, Solna, Sweden.
AD  - Department of Orthopaedics Eksjö, Regional Hospital Eksjö, Region Jönköping County, 
      Sweden.
AD  - Department of Biomedical and Clinical Sciences, Linköping University, Linköping, 
      Sweden.
FAU - Peterson, Charlotte A
AU  - Peterson CA
AD  - Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
AD  - Department of Physical Therapy, University of Kentucky, Lexington, KY, USA.
FAU - McCarthy, John J
AU  - McCarthy JJ
AD  - Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
AD  - Department of Physiology, University of Kentucky, Lexington, KY, USA.
LA  - eng
GR  - R01DK119619/HHS | NIH | National Institute of Diabetes and Digestive and Kidney 
      Diseases (NIDDK)/
GR  - RJC | Futurum - Akademin för Hälsa och Vård, Region Jönköpings läns (Futurum)/
GR  - Svenska Forskningsrådet Formas (Swedish Research Council Formas)/
PT  - Journal Article
PL  - United States
TA  - FASEB J
JT  - FASEB journal : official publication of the Federation of American Societies for 
      Experimental Biology
JID - 8804484
SB  - IM
OTO - NOTNLM
OT  - adipose tissue
OT  - extracellular vesicles
OT  - lipolysis
OT  - microRNAs
OT  - skeletal muscle
EDAT- 2021/05/26 06:00
MHDA- 2021/05/26 06:00
CRDT- 2021/05/25 14:09
PHST- 2021/04/02 00:00 [revised]
PHST- 2021/02/09 00:00 [received]
PHST- 2021/04/19 00:00 [accepted]
PHST- 2021/05/25 14:09 [entrez]
PHST- 2021/05/26 06:00 [pubmed]
PHST- 2021/05/26 06:00 [medline]
AID - 10.1096/fj.202100242R [doi]
PST - ppublish
SO  - FASEB J. 2021 Jun;35(6):e21644. doi: 10.1096/fj.202100242R.

PMID- 34032694
OWN - NLM
STAT- In-Process
LR  - 20210529
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 100
IP  - 21
DP  - 2021 May 28
TI  - miR-96-5p: A potential diagnostic marker for gestational diabetes mellitus.
PG  - e25808
LID - 10.1097/MD.0000000000025808 [doi]
LID - e25808
AB  - MicroRNAs play important roles in gestational diabetes mellitus (GDM), and this 
      study aimed to elucidate the clinical significance of miR-96-5p in diagnosing 
      GDM.There are 123 pregnant women diagnosed with GDM and 123 healthy pregnant women 
      were enrolled as control participants. Placenta and plasma samples from the patients 
      and control participants were collected, and quantitative reverse transcription 
      polymerase chain reaction (RT-qPCR) was performed to determine miR-96-5p expression 
      levels. Moreover, a receiver operating characteristic (ROC) curve was established to 
      evaluate the significance of miR-96-5p in diagnosing GDM. HRT-8/SVneo trophoblasts 
      were cultured under high glucose conditions and treated with miR-96-5p mimics, and 
      cell viability was examined.miR-96-5p levels were significantly decreased in both 
      the placenta and plasma samples of patients with GDM. The ROC curve indicated that 
      miR-96-5p can serve as a diagnostic biomarker for GDM with high sensitivity and 
      specificity. Moreover, miR-96-5p levels were markedly low under high glucose 
      conditions, and the overexpression of miR-96-5p increased the viability, 
      respectively, of trophoblasts in vitro.miR-96-5p may participate in the pathogenesis 
      of GDM by exerting effects on the viability of trophoblasts.
CI  - Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.
FAU - Yu, Xinyang
AU  - Yu X
AUID- ORCID: 0000-0002-1799-1192
AD  - Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing 
      Medicine University, Chongqing, China.
FAU - Liu, Zhengfei
AU  - Liu Z
AUID- ORCID: 0000-0001-8161-3420
FAU - Fang, Jie
AU  - Fang J
AUID- ORCID: 0000-0003-3786-1704
FAU - Qi, Hongbo
AU  - Qi H
AUID- ORCID: 0000-0002-4268-344
LA  - eng
GR  - CXTDX201601014/Innovation team Foundation of Chongqing Education Commission/
PT  - Journal Article
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
SB  - AIM
SB  - IM
PMC - PMC8154478
COIS- The authors have no conflicts of interest to disclose.
EDAT- 2021/05/26 06:00
MHDA- 2021/05/26 06:00
CRDT- 2021/05/25 13:55
PHST- 2020/10/13 00:00 [received]
PHST- 2021/04/15 00:00 [accepted]
PHST- 2021/05/25 13:55 [entrez]
PHST- 2021/05/26 06:00 [pubmed]
PHST- 2021/05/26 06:00 [medline]
AID - 00005792-202105280-00004 [pii]
AID - MD-D-20-10091 [pii]
AID - 10.1097/MD.0000000000025808 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2021 May 28;100(21):e25808. doi: 10.1097/MD.0000000000025808.

PMID- 34029597
OWN - NLM
STAT- Publisher
LR  - 20210524
IS  - 1532-8600 (Electronic)
IS  - 0026-0495 (Linking)
DP  - 2021 May 21
TI  - Diabetes and kidney disease: emphasis on treatment with SGLT-2 inhibitors and GLP-1 
      receptor agonists.
PG  - 154799
LID - S0026-0495(21)00099-8 [pii]
LID - 10.1016/j.metabol.2021.154799 [doi]
AB  - Kidney disease is a frequent microvascular complication of both type 1 and type 2 
      diabetes. Historic trials have demonstrated that a tight glycaemic control is the 
      most powerful approach to decrease the chances of developing diabetic nephropathy. 
      However, having an HbA1c < 7% does not completely suppress the risk of kidney 
      disease. The observed residual risk is likely ascribable to two phenomena: 1- the 
      presence of risk factors and alterations additive to and independent of glycaemia, 
      and 2- the activation of long-lasting imbalances by periods of exposure to 
      uncontrolled glycemia, a phenomenon referred to as metabolic memory or legacy 
      effect. Long-lasting oxidative stress, epigenetic alterations, cellular senescence, 
      and the resulting chronic low-grade inflammation are all candidate mechanisms 
      explaining the development of nephropathy despite proper control of risk factors. 
      Recently, two classes of drugs, i.e. glucagon-like peptide (GLP) 1 receptor agonists 
      (RA) and sodium-glucose transporter 2 inhibitors (SGLT-i) have changed this 
      scenario. Indeed, cardiovascular outcome and other trials have clearly shown a 
      renoprotective effect for these drugs, well-beyond their glucose-lowering 
      properties. In this review, we summarize: 1- selected key trials and mechanisms 
      underlying the development of diabetic kidney disease and 2- the results relative to 
      renal endpoints in clinical trials of GLP-1 RA and SGLT-2i. Then, we briefly discuss 
      some of the hypotheses posited to explain the marked renoprotective properties of 
      these two classes, evidencing the still existing gaps in knowledge and proposing 
      future directions to further implement the use of these powerful, disease-modifying 
      drugs.
CI  - Copyright © 2021 Elsevier Inc. All rights reserved.
FAU - Prattichizzo, Francesco
AU  - Prattichizzo F
AD  - IRCCS MultiMedica, Milan, Italy. Electronic address: 
      francesco.prattichizzo@multimedica.it.
FAU - de Candia, Paola
AU  - de Candia P
AD  - IRCCS MultiMedica, Milan, Italy.
FAU - Ceriello, Antonio
AU  - Ceriello A
AD  - IRCCS MultiMedica, Milan, Italy.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20210521
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
SB  - IM
OTO - NOTNLM
OT  - Blood pressure
OT  - Diabetes complications
OT  - Diabetes mellitus
OT  - Diabetes treatment algorithm
OT  - Epigenetics
OT  - GLP-1
OT  - Glucose control
OT  - Low-grade inflammation
OT  - Nephropathy
OT  - Oxidative stress
OT  - SGLT-2
OT  - miRNAs
EDAT- 2021/05/25 06:00
MHDA- 2021/05/25 06:00
CRDT- 2021/05/24 20:22
PHST- 2021/04/01 00:00 [received]
PHST- 2021/05/06 00:00 [revised]
PHST- 2021/05/17 00:00 [accepted]
PHST- 2021/05/24 20:22 [entrez]
PHST- 2021/05/25 06:00 [pubmed]
PHST- 2021/05/25 06:00 [medline]
AID - S0026-0495(21)00099-8 [pii]
AID - 10.1016/j.metabol.2021.154799 [doi]
PST - aheadofprint
SO  - Metabolism. 2021 May 21:154799. doi: 10.1016/j.metabol.2021.154799.

PMID- 34028994
OWN - NLM
STAT- Publisher
LR  - 20210524
IS  - 1748-1716 (Electronic)
IS  - 1748-1708 (Linking)
DP  - 2021 May 24
TI  - MiR-205 is upregulated in islets of diabetes-susceptible mice and targets the 
      diabetes gene Tcf7l2.
PG  - e13693
LID - 10.1111/apha.13693 [doi]
AB  - AIM: MicroRNAs play an important role in the maintenance of cellular functions by 
      fine-tuning gene expression levels. The aim of the current study was to identify 
      genetically caused changes in microRNA expression which associate with islet 
      dysfunction in diabetic mice. METHODS: To identify novel microRNAs involved in islet 
      dysfunction, transcriptome and miRNome analyses were performed in islets of obese, 
      diabetes-susceptible NZO and diabetes-resistant B6-ob/ob mice and results combined 
      with quantitative trait loci (QTL) and functional in vitro analysis. RESULTS: In 
      islets of NZO and B6-ob/ob mice 94 differentially expressed microRNAs were detected, 
      of which 11 are located in diabetes QTL. Focusing on conserved microRNAs exhibiting 
      the strongest expression difference and which have not been linked to islet 
      function, miR-205-5p was selected for further analysis. According to transcriptome 
      data and target prediction analyses, miR-205-5p affects genes involved in Wnt and 
      calcium signalling as well as insulin secretion. Overexpression of miR-205-5p in the 
      insulinoma cell line INS-1 increased insulin expression and basal insulin secretion 
      and supressed the expression of the diabetes gene TCF7L2. The interaction between 
      miR-205-5p and TCF7L2 was confirmed by luciferase reporter assay. CONCLUSION: 
      MiR-205-5p was identified as relevant microRNA involved in islet dysfunction by 
      interacting with TCF7L2.
CI  - This article is protected by copyright. All rights reserved.
FAU - Ouni, Meriem
AU  - Ouni M
AUID- ORCID: 0000-0002-7781-8463
AD  - Department of Experimental Diabetology, German Institute of Human Nutrition 
      Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
AD  - German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
FAU - Gottmann, Pascal
AU  - Gottmann P
AD  - Department of Experimental Diabetology, German Institute of Human Nutrition 
      Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
AD  - German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
FAU - Westholm, Efraim
AU  - Westholm E
AUID- ORCID: 0000-0002-2383-8549
AD  - Department of Experimental Diabetology, German Institute of Human Nutrition 
      Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
AD  - Lund University Diabetes Centre, Unit of Islet Cell Exocytosis, Department of 
      Clinical Sciences Malmö, Lund University, Sweden.
FAU - Schwerbel, Kristin
AU  - Schwerbel K
AD  - Department of Experimental Diabetology, German Institute of Human Nutrition 
      Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
AD  - German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
FAU - Jähnert, Markus
AU  - Jähnert M
AD  - Department of Experimental Diabetology, German Institute of Human Nutrition 
      Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
AD  - German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
FAU - Stadion, Mandy
AU  - Stadion M
AD  - Department of Experimental Diabetology, German Institute of Human Nutrition 
      Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
AD  - German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
FAU - Rittig, Kilian
AU  - Rittig K
AD  - Clinic for Angiology and Diabetology, 15236, Frankfurt (Oder), Germany.
AD  - University of Potsdam, Institute of Nutritional Science, Germany.
FAU - Vogel, Heike
AU  - Vogel H
AD  - Department of Experimental Diabetology, German Institute of Human Nutrition 
      Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
AD  - German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
AD  - Research Group Genetics of obesity, German Institute of Human Nutrition 
      Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
AD  - Research Group Molecular and Clinical Life Science of Metabolic Diseases, Faculty of 
      Health Sciences Brandenburg, University of Potsdam, Germany.
FAU - Schürmann, Annette
AU  - Schürmann A
AD  - Department of Experimental Diabetology, German Institute of Human Nutrition 
      Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
AD  - German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
AD  - University of Potsdam, Institute of Nutritional Science, Germany.
LA  - eng
PT  - Journal Article
DEP - 20210524
PL  - England
TA  - Acta Physiol (Oxf)
JT  - Acta physiologica (Oxford, England)
JID - 101262545
SB  - IM
OTO - NOTNLM
OT  - Tcf7l2
OT  - GSIS
OT  - Islets of Langerhans
OT  - MicroRNA
OT  - T2D
EDAT- 2021/05/25 06:00
MHDA- 2021/05/25 06:00
CRDT- 2021/05/24 12:49
PHST- 2021/05/24 12:49 [entrez]
PHST- 2021/05/25 06:00 [pubmed]
PHST- 2021/05/25 06:00 [medline]
AID - 10.1111/apha.13693 [doi]
PST - aheadofprint
SO  - Acta Physiol (Oxf). 2021 May 24:e13693. doi: 10.1111/apha.13693.

PMID- 34028435
OWN - NLM
STAT- In-Data-Review
LR  - 20210525
IS  - 1940-087X (Electronic)
IS  - 1940-087X (Linking)
IP  - 171
DP  - 2021 May 4
TI  - An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA 
      Modulation on Adipocyte Function.
LID - 10.3791/61925 [doi]
AB  - Alteration of adipocyte function contributes to the pathogenesis of metabolic 
      diseases including Type 2 diabetes and insulin resistance. This highlights the need 
      to better understand the molecular mechanism involved in adipocyte dysfunction to 
      develop new therapies against obesity-related diseases. Modulating the expression of 
      proteins and micro-RNAs in adipocytes remains highly challenging. This paper 
      describes a protocol to differentiate murine fibroblasts into mature adipocytes and 
      to modulate the expression of proteins and micro-RNAs in mature adipocytes through 
      reverse-transfection using small-interfering RNA (siRNA) and micro-RNA mimicking 
      (miR mimic) oligonucleotides. This reverse-transfection protocol involves the 
      incubation of the transfection reagent and the oligonucleotides to form a complex in 
      the cell culture plate to which the mature adipocytes are added. The adipocytes are 
      then allowed to reattach to the adherent plate surface in the presence of the 
      oligonucleotides/transfection reagent complex. Functional analyses such as the study 
      of insulin signaling, glucose uptake, lipogenesis, and lipolysis can be performed on 
      the transfected 3T3-L1 mature adipocytes to study the impact of protein or micro-RNA 
      manipulation on adipocyte function.
FAU - Jager, Jennifer
AU  - Jager J
AD  - Université Côte d'Azur, Inserm, C3M, Team Cellular and Molecular Pathophysiology of 
      Obesity and Diabetes, Nice, France; jennifer.jager@unice.fr.
FAU - Gaudfrin, Mélanie
AU  - Gaudfrin M
AD  - Université Côte d'Azur, Inserm, C3M, Team Cellular and Molecular Pathophysiology of 
      Obesity and Diabetes, Nice, France.
FAU - Gilleron, Jérôme
AU  - Gilleron J
AD  - Université Côte d'Azur, Inserm, C3M, Team Cellular and Molecular Pathophysiology of 
      Obesity and Diabetes, Nice, France.
FAU - Cormont, Mireille
AU  - Cormont M
AD  - Université Côte d'Azur, Inserm, C3M, Team Cellular and Molecular Pathophysiology of 
      Obesity and Diabetes, Nice, France.
FAU - Tanti, Jean-François
AU  - Tanti JF
AD  - Université Côte d'Azur, Inserm, C3M, Team Cellular and Molecular Pathophysiology of 
      Obesity and Diabetes, Nice, France.
LA  - eng
PT  - Journal Article
PT  - Video-Audio Media
DEP - 20210504
PL  - United States
TA  - J Vis Exp
JT  - Journal of visualized experiments : JoVE
JID - 101313252
SB  - IM
EDAT- 2021/05/25 06:00
MHDA- 2021/05/25 06:00
CRDT- 2021/05/24 12:27
PHST- 2021/05/24 12:27 [entrez]
PHST- 2021/05/25 06:00 [pubmed]
PHST- 2021/05/25 06:00 [medline]
AID - 10.3791/61925 [doi]
PST - epublish
SO  - J Vis Exp. 2021 May 4;(171). doi: 10.3791/61925.

PMID- 34024846
OWN - NLM
STAT- Publisher
LR  - 20210524
IS  - 1348-4540 (Electronic)
IS  - 0918-8959 (Linking)
DP  - 2021 May 21
TI  - Exosomes from mesenchymal stem cells expressing microribonucleic acid-125b inhibit 
      the progression of diabetic nephropathy via the tumour necrosis factor 
      receptor-associated factor 6/Akt axis.
LID - 10.1507/endocrj.EJ20-0619 [doi]
AB  - Diabetic nephropathy (DN) seriously threatens the health of patients with diabetes. 
      Moreover, it has been reported that mesenchymal stem cell (MSC)-derived exosomal 
      miRNAs can modulate the progression of multiple diseases, including DN. It has been 
      suggested that miR-125b is involved in DN. However, the biological functions of 
      exosomal miRNAs, especially miR-125b, in DN are still unclear. To establish a DN 
      model in vitro, we used a model of human embryonic kidney epithelial cells (HKCs) 
      injury induced by high glucose (HG). Then, miR-125b was delivered to the model cells 
      in vitro via MSC-derived exosomes (MSC-Exos), and the effect of exosomal miR-125b on 
      HKCs apoptosis was evaluated by flow cytometry. qRT-PCR or western blotting was 
      performed to measure miR-125b or tumour necrosis factor receptor-associated factor 6 
      (TRAF6) expression in HKC. The effect of MSC-Exos on HKCs apoptosis after miR-125b 
      knockdown was determined by flow cytometry. Moreover, dual-luciferase reporter 
      assays were used to determine the targeting relationship between miR-125b and TRAF6 
      in HKCs. Our data revealed that MSC-Exos increased HG-induced autophagy in HKCs and 
      reversed HKCs apoptosis. Moreover, our study found that miR-125b was enriched in 
      MSC-Exos and directly targeted TRAF6 in HKCs. In addition, exosomally transferred 
      miR-125b inhibited the apoptosis of HG-treated HKCs by mediating Akt signalling. In 
      summary, MSC-derived exosomal miR-125b induced autophagy and inhibited apoptosis in 
      HG-treated HKCs via the downregulation of TRAF6. Therefore, our study provided a new 
      idea for DN treatment.
FAU - Cai, Xia
AU  - Cai X
AD  - Department of Endocrinology, The Second Affiliated Hospital of Nanchang University, 
      Nanchang 330006, Jiangxi Province, P.R.China.
FAU - Zou, Fang
AU  - Zou F
AD  - Department of Endocrinology, The Second Affiliated Hospital of Nanchang University, 
      Nanchang 330006, Jiangxi Province, P.R.China.
FAU - Xuan, Rui
AU  - Xuan R
AD  - Department of Endocrinology, The Second Affiliated Hospital of Nanchang University, 
      Nanchang 330006, Jiangxi Province, P.R.China.
FAU - Lai, Xiao-Yang
AU  - Lai XY
AD  - Department of Endocrinology, The Second Affiliated Hospital of Nanchang University, 
      Nanchang 330006, Jiangxi Province, P.R.China.
LA  - eng
PT  - Journal Article
DEP - 20210521
PL  - Japan
TA  - Endocr J
JT  - Endocrine journal
JID - 9313485
SB  - IM
OTO - NOTNLM
OT  - Apoptosis
OT  - Autophagy
OT  - Diabetic nephropathy
OT  - miR-125b
EDAT- 2021/05/25 06:00
MHDA- 2021/05/25 06:00
CRDT- 2021/05/24 07:54
PHST- 2021/05/24 07:54 [entrez]
PHST- 2021/05/25 06:00 [pubmed]
PHST- 2021/05/25 06:00 [medline]
AID - 10.1507/endocrj.EJ20-0619 [doi]
PST - aheadofprint
SO  - Endocr J. 2021 May 21. doi: 10.1507/endocrj.EJ20-0619.

PMID- 34017372
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210523
IS  - 1943-8141 (Print)
IS  - 1943-8141 (Electronic)
IS  - 1943-8141 (Linking)
VI  - 13
IP  - 4
DP  - 2021
TI  - Protective mechanism of apigenin in diabetic nephropathy is related to its 
      regulation of miR-423-5P-USF2 axis.
PG  - 2006-2020
AB  - Apigenin (APG), a natural flavonoid with anti-inflammatory and anti-fibrosis 
      properties, has been shown to play a protective role in diabetic nephropathy (DN), 
      but their molecular protection mechanism for miRNA has not been elucidated in 
      detail. This study was designed to focus on exploring its protective role in DN and 
      whether miR-423-5p-upstream stimulating factor 2 (USF2) axis was involved in its 
      protective mechanism. The in vivo model of rat was induced by streptozotocin (STZ) 
      and the in vitro model of renal tubular epithelial cell (RTEC) was induced by high 
      glucose (HG). Our in vivo study revealed that APG had different protective effects 
      on inflammation, renal fibrosis and epithelial mesenchymal transition (EMT) in DN 
      rats, which is mainly reflected in that the inflammatory factors (IL-6, IFN-γ, 
      TNF-α) were obviously down-regulated, the renal fibrosis markers (IV-C, FN, Col I) 
      were significantly inhibited, the E-cadherin (EMT factors) was significantly 
      up-regulated, while the vimentin and α-SMA (EMT factors) were significantly 
      down-regulated, and the renal function indexes (serum Cr, BUN) were significantly 
      improved. In terms of mechanism, the protective effect of APG was related to the 
      regulation of the expression of miR-423-5p-USF2 axis, and there was a targeted 
      relationship between miR-423-5p and USF2. Down-regulating miR-423-5p or 
      up-regulating USF2 could significantly aggravate the disease progression of in vitro 
      model and eliminate DN resistance under APG intervention. The above results revealed 
      that the protective role of APG on DN was mediated by miR-423-5p-USF2 axis.
CI  - AJTR Copyright © 2021.
FAU - Hou, Yi
AU  - Hou Y
AD  - Department of Urology, China-Japan Union Hospital of Jilin University Changchun 
      130033, Jilin, P. R. China.
FAU - Zhang, Yan
AU  - Zhang Y
AD  - Department of Endocrinology, China-Japan Union Hospital of Jilin University 
      Changchun 130033, Jilin, P. R. China.
FAU - Lin, Sitong
AU  - Lin S
AD  - Department of Endocrinology, China-Japan Union Hospital of Jilin University 
      Changchun 130033, Jilin, P. R. China.
FAU - Yu, Yue
AU  - Yu Y
AD  - Department of Endocrinology, China-Japan Union Hospital of Jilin University 
      Changchun 130033, Jilin, P. R. China.
FAU - Yang, Liu
AU  - Yang L
AD  - Department of Endocrinology, China-Japan Union Hospital of Jilin University 
      Changchun 130033, Jilin, P. R. China.
FAU - Li, Lei
AU  - Li L
AD  - Department of Urology, China-Japan Union Hospital of Jilin University Changchun 
      130033, Jilin, P. R. China.
FAU - Wang, Wenxiang
AU  - Wang W
AD  - Department of Urology, China-Japan Union Hospital of Jilin University Changchun 
      130033, Jilin, P. R. China.
LA  - eng
PT  - Journal Article
DEP - 20210415
TA  - Am J Transl Res
JT  - American journal of translational research
JID - 101493030
PMC - PMC8129299
OTO - NOTNLM
OT  - Diabetic nephropathy
OT  - USF2
OT  - apigenin
OT  - inflammation/renal fibrosis/epithelial mesenchymal transition
OT  - miR-423-5p
COIS- None.
EDAT- 2021/05/22 06:00
MHDA- 2021/05/22 06:01
CRDT- 2021/05/21 06:31
PHST- 2020/11/09 00:00 [received]
PHST- 2021/01/04 00:00 [accepted]
PHST- 2021/05/21 06:31 [entrez]
PHST- 2021/05/22 06:00 [pubmed]
PHST- 2021/05/22 06:01 [medline]
PST - epublish
SO  - Am J Transl Res. 2021 Apr 15;13(4):2006-2020. eCollection 2021.

PMID- 34017037
OWN - NLM
STAT- In-Data-Review
LR  - 20210526
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 11
IP  - 1
DP  - 2021 May 20
TI  - Whole transcriptome RNA-seq reveals key regulatory factors involved in type 2 
      diabetes pathology in peripheral fat of Asian Indians.
PG  - 10632
LID - 10.1038/s41598-021-90148-z [doi]
LID - 10632
AB  - The prevalence of Type 2 Diabetes has reached an epidemic proportion particularly in 
      south Asian countries. We have earlier shown that the anatomical fat distribution, 
      termed 'thin fat phenotype' in this population indeed plays a major role for their 
      T2D-predisposition it is indeed the sick fat or adiposopathy, which is the root 
      cause of metabolic syndrome and diabetes and affects both-peripheral, as well as 
      visceral adipose tissue compartments. In present study, we have attempted to unravel 
      the altered regulatory mechanisms at the level of transcription factors, and miRNAs 
      those may likely accounts to T2D pathophysiology in femoral subcutaneous adipose 
      tissue. We prioritized transcription factors and protein kinases as likely upstream 
      regulators of obtained differentially expressed genes in this RNA-seq study. An 
      inferred network of these upstream regulators was then derived and the role of TFs 
      and miRNAs in T2D pathophysiology was explored. In conclusions, this RNS-Seq study 
      finds that peripheral subcutaneous adipose tissue among Asian Indians show pathology 
      characterized by altered lipid, glucose and protein metabolism, adipogenesis defect 
      and inflammation. A network of regulatory transcription factors, protein kinases and 
      microRNAs have been imputed which converge on the process of adipogenesis. As the 
      majority of these genes also showed altered expression in diabetics and some of them 
      are also circulatory, therefore they deserve further investigation for potential 
      clinical diagnostic and therapeutic applications.
FAU - Saxena, Aditya
AU  - Saxena A
AD  - Department of Computer Engineering and Applications, Institute of Engineering and 
      Technology, GLA University, Mathura, 281406, India.
FAU - Mathur, Nitish
AU  - Mathur N
AD  - Department of Endocrinology, Sawai Man Singh Medical College and Hospital, Jaipur, 
      302004, India.
FAU - Tiwari, Pradeep
AU  - Tiwari P
AD  - Department of Endocrinology, Sawai Man Singh Medical College and Hospital, Jaipur, 
      302004, India.
AD  - Department of Chemistry, School of Basic Sciences, Manipal University Jaipur, 
      Jaipur, 303007, India.
FAU - Mathur, Sandeep Kumar
AU  - Mathur SK
AD  - Department of Endocrinology, Sawai Man Singh Medical College and Hospital, Jaipur, 
      302004, India. drsandeepmathur@rediffmail.com.
LA  - eng
PT  - Journal Article
DEP - 20210520
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
SB  - IM
PMC - PMC8137704
COIS- The authors declare no competing interests.
EDAT- 2021/05/22 06:00
MHDA- 2021/05/22 06:00
CRDT- 2021/05/21 06:19
PHST- 2021/02/02 00:00 [received]
PHST- 2021/05/06 00:00 [accepted]
PHST- 2021/05/21 06:19 [entrez]
PHST- 2021/05/22 06:00 [pubmed]
PHST- 2021/05/22 06:00 [medline]
AID - 10.1038/s41598-021-90148-z [pii]
AID - 90148 [pii]
AID - 10.1038/s41598-021-90148-z [doi]
PST - epublish
SO  - Sci Rep. 2021 May 20;11(1):10632. doi: 10.1038/s41598-021-90148-z.

PMID- 34016957
OWN - NLM
STAT- In-Data-Review
LR  - 20210521
IS  - 2041-4889 (Electronic)
VI  - 12
IP  - 6
DP  - 2021 May 20
TI  - Let-7f miRNA regulates SDF-1α- and hypoxia-promoted migration of mesenchymal stem 
      cells and attenuates mammary tumor growth upon exosomal release.
PG  - 516
LID - 10.1038/s41419-021-03789-3 [doi]
AB  - Bone marrow-derived human mesenchymal stem cells (hMSCs) are recruited to damaged or 
      inflamed tissues where they contribute to tissue repair. This multi-step process 
      involves chemokine-directed invasion of hMSCs and on-site release of factors that 
      influence target cells or tumor tissues. However, the underlying molecular 
      mechanisms are largely unclear. Previously, we described that microRNA let-7f 
      controls hMSC differentiation. Here, we investigated the role of let-7f in 
      chemotactic invasion and paracrine anti-tumor effects. Incubation with stromal 
      cell-derived factor-1α (SDF-1α) or inflammatory cytokines upregulated let-7f 
      expression in hMSCs. Transfection of hMSCs with let-7f mimics enhanced 
      CXCR4-dependent invasion by augmentation of pericellular proteolysis and release of 
      matrix metalloproteinase-9. Hypoxia-induced stabilization of the hypoxia-inducible 
      factor 1 alpha in hMSCs promoted cell invasion via let-7f and activation of 
      autophagy. Dependent on its endogenous level, let-7f facilitated hMSC motility and 
      invasion through regulation of the autophagic flux in these cells. In addition, 
      secreted let-7f encapsulated in exosomes was increased upon upregulation of 
      endogenous let-7f by treatment of the cells with SDF-1α, hypoxia, or induction of 
      autophagy. In recipient 4T1 tumor cells, hMSC-derived exosomal let-7f attenuated 
      proliferation and invasion. Moreover, implantation of 3D spheroids composed of hMSCs 
      and 4T1 cells into a breast cancer mouse model demonstrated that hMSCs 
      overexpressing let-7f inhibited tumor growth in vivo. Our findings provide evidence 
      that let-7f is pivotal in the regulation of hMSC invasion in response to 
      inflammation and hypoxia, suggesting that exosomal let-7f exhibits paracrine 
      anti-tumor effects.
FAU - Egea, Virginia
AU  - Egea V
AUID- ORCID: 0000-0003-4759-3408
AD  - Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University of 
      Munich, Munich, Germany. virginia.egea@med.uni-muenchen.de.
FAU - Kessenbrock, Kai
AU  - Kessenbrock K
AD  - Department of Anatomy, University of California, San Francisco, CA, USA.
FAU - Lawson, Devon
AU  - Lawson D
AD  - Department of Anatomy, University of California, San Francisco, CA, USA.
FAU - Bartelt, Alexander
AU  - Bartelt A
AD  - Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University of 
      Munich, Munich, Germany.
AD  - German Center for Cardiovascular Research (DZHK), Partner Site Munich Heart 
      Alliance, Munich, Germany.
AD  - Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, 
      Germany.
AD  - Department of Molecular Metabolism, 665 Huntington Avenue, Harvard T.H. Chan School 
      of Public Health, 02115, Boston, MA, USA.
FAU - Weber, Christian
AU  - Weber C
AD  - Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University of 
      Munich, Munich, Germany.
AD  - Dept. Biochemistry, Cardiovascular Research Institute Maastricht, University of 
      Maastricht, Maastricht, The Netherlands.
AD  - Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.
FAU - Ries, Christian
AU  - Ries C
AD  - Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University of 
      Munich, Munich, Germany. christian.ries@med.uni-muenchen.de.
LA  - eng
GR  - Junior Research Group Grant/Deutsches Zentrum für Herz-Kreislaufforschung (Deutsches 
      Zentrum für Herz-Kreislaufforschung e.V.)/
GR  - RI 808/6-1/Deutsche Forschungsgemeinschaft (German Research Foundation)/
PT  - Journal Article
DEP - 20210520
PL  - England
TA  - Cell Death Dis
JT  - Cell death & disease
JID - 101524092
SB  - IM
EDAT- 2021/05/22 06:00
MHDA- 2021/05/22 06:00
CRDT- 2021/05/21 06:05
PHST- 2021/01/14 00:00 [received]
PHST- 2021/05/03 00:00 [accepted]
PHST- 2021/05/03 00:00 [revised]
PHST- 2021/05/21 06:05 [entrez]
PHST- 2021/05/22 06:00 [pubmed]
PHST- 2021/05/22 06:00 [medline]
AID - 10.1038/s41419-021-03789-3 [pii]
AID - 10.1038/s41419-021-03789-3 [doi]
PST - epublish
SO  - Cell Death Dis. 2021 May 20;12(6):516. doi: 10.1038/s41419-021-03789-3.

PMID- 34014023
OWN - NLM
STAT- Publisher
LR  - 20210520
IS  - 1522-7278 (Electronic)
IS  - 1520-4081 (Linking)
DP  - 2021 May 20
TI  - MiR-17-5p downregulation alleviates apoptosis and fibrosis in high glucose-induced 
      human mesangial cells through inactivation of Wnt/β-catenin signaling by targeting 
      KIF23.
LID - 10.1002/tox.23280 [doi]
AB  - Diabetic nephropathy (DN) remains the major cause of end-stage renal disease. 
      MicroRNAs (miRNAs) have been reported to perform biological functions in many 
      diseases. This investigation elucidated the biological role of miR-17-5p in DN. In 
      this study, high glucose-cultured human mesangial cells (HMCs) were used as a cell 
      model of DN. The miR-17-5p and KIF23 expression was measured by RT-qPCR. Cell 
      apoptosis was detected by flow cytometry. The protein levels of apoptosis markers, 
      fibrosis markers, and Wnt/β-catenin signaling-related genes were assessed using 
      western blotting. The interaction of miR-17-5p with KIF23 was tested by a luciferase 
      reporter assay. We found that miR-17-5p was upregulated in both DN patients and high 
      glucose-treated HMCs. Silencing miR-17-5p attenuated the apoptosis and fibrosis in 
      high glucose-treated HMCs. MiR-17-5p binds to KIF23 3'UTR and negatively regulates 
      KIF23 expression. KIF23 knockdown could suppress the role of miR-17-5p inhibition in 
      high glucose-treated HMCs. Additionally, inhibition of miR-17-5p activated 
      Wnt/β-catenin signaling in HMCs through upregulating KIF23 expression. Suppression 
      of Wnt/β-catenin signaling antagonized the effect of miR-17-5p in HMCs. In 
      conclusion, miR-17-5p inhibition alleviates the apoptosis and fibrosis in high 
      glucose-treated HMCs by targeting KIF23 activating Wnt/β-catenin signaling.
CI  - © 2021 Wiley Periodicals LLC.
FAU - Chen, Xiaoli
AU  - Chen X
AD  - Department of Endocrinology, The Affiliated Zhangjiagang Hospital of Soochow 
      University, Suzhou, Jiangsu, China.
FAU - Gu, Liyan
AU  - Gu L
AD  - Department of Endocrinology, The Affiliated Zhangjiagang Hospital of Soochow 
      University, Suzhou, Jiangsu, China.
FAU - Chen, Xia
AU  - Chen X
AD  - Department of Endocrinology, The Affiliated Zhangjiagang Hospital of Soochow 
      University, Suzhou, Jiangsu, China.
FAU - Xing, Jianping
AU  - Xing J
AD  - Department of Endocrinology, The Affiliated Zhangjiagang Hospital of Soochow 
      University, Suzhou, Jiangsu, China.
FAU - Zhang, Chengxia
AU  - Zhang C
AUID- ORCID: 0000-0002-4761-8524
AD  - Department of Endocrinology, The Affiliated Zhangjiagang Hospital of Soochow 
      University, Suzhou, Jiangsu, China.
LA  - eng
PT  - Journal Article
DEP - 20210520
PL  - United States
TA  - Environ Toxicol
JT  - Environmental toxicology
JID - 100885357
SB  - IM
OTO - NOTNLM
OT  - KIF23
OT  - Wnt/β-catenin signaling
OT  - diabetic nephropathy
OT  - miR-17-5p
EDAT- 2021/05/21 06:00
MHDA- 2021/05/21 06:00
CRDT- 2021/05/20 09:01
PHST- 2021/04/28 00:00 [revised]
PHST- 2021/03/10 00:00 [received]
PHST- 2021/05/05 00:00 [accepted]
PHST- 2021/05/20 09:01 [entrez]
PHST- 2021/05/21 06:00 [pubmed]
PHST- 2021/05/21 06:00 [medline]
AID - 10.1002/tox.23280 [doi]
PST - aheadofprint
SO  - Environ Toxicol. 2021 May 20. doi: 10.1002/tox.23280.

PMID- 34011169
OWN - NLM
STAT- Publisher
LR  - 20210520
IS  - 1557-7716 (Electronic)
IS  - 1523-0864 (Linking)
DP  - 2021 May 19
TI  - Reactive oxygen species mediated diabetic heart disease - mechanisms and therapies.
LID - 10.1089/ars.2021.0098 [doi]
AB  - Significance: Diabetic heart disease (DHD) is the primary cause of mortality in 
      people with diabetes. A significant contributor to the development of DHD is the 
      disruption of redox balance due to reactive oxygen species (ROS) overproduction 
      resulting from sustained high glucose levels. Therapies specifically focusing on 
      suppression of ROS will hugely benefit patients with DHD. Recent Advances: In 
      addition to the gold standard pharmacological therapies, the recent development of 
      gene therapy provides an exciting avenue for developing new therapeutics to treat 
      ROS mediated DHD. In particular, microRNAs (miRNAs) are gaining interest due to 
      their crucial role in several physiological and pathological processes, including 
      DHD. Critical Issues: miRNAs have many targets and differential function depending 
      on the environment. Therefore, a proper understanding of the function of miRNAs in 
      specific cell types and cell states is required for the successful application of 
      this technology. In the present review, we will first provide an overview of the 
      role of ROS in contributing to DHD and the currently available treatments. We will 
      then discuss the newer gene therapies with a specific focus on the role of miRNAs as 
      the causative factors and therapeutic targets to combat ROS mediated DHD. Future 
      Directions: The future of miRNA therapeutics in tackling ROS mediated DHD is 
      dependent on a complete understanding of how miRNAs behave in different cells and 
      environments. Future research should also aim to develop conditional miRNA 
      therapeutic platforms capable of switching on and off in response to disruptions in 
      the redox state.
FAU - Reily-Bell, Matthew
AU  - Reily-Bell M
AD  - University of Otago, 2495, Physiology-HeartOtago, Dunedin, New Zealand; 
      mattyjbel@gmail.com.
FAU - Bahn, Andrew
AU  - Bahn A
AD  - University of Otago, 2495, Physiology, Dunedin, New Zealand; 
      andrew.bahn@otago.ac.nz.
FAU - Katare, Rajesh
AU  - Katare R
AD  - University of Otago, 2495, Physiology-HeartOtago, Dunedin, New Zealand; 
      rajesh.katare@otago.ac.nz.
LA  - eng
PT  - Journal Article
DEP - 20210519
PL  - United States
TA  - Antioxid Redox Signal
JT  - Antioxidants & redox signaling
JID - 100888899
SB  - IM
EDAT- 2021/05/21 06:00
MHDA- 2021/05/21 06:00
CRDT- 2021/05/20 05:31
PHST- 2021/05/20 05:31 [entrez]
PHST- 2021/05/21 06:00 [pubmed]
PHST- 2021/05/21 06:00 [medline]
AID - 10.1089/ars.2021.0098 [doi]
PST - aheadofprint
SO  - Antioxid Redox Signal. 2021 May 19. doi: 10.1089/ars.2021.0098.

PMID- 34009437
OWN - NLM
STAT- Publisher
LR  - 20210519
IS  - 1432-5233 (Electronic)
IS  - 0940-5429 (Linking)
DP  - 2021 May 19
TI  - MicroRNAs modulation and clinical outcomes at 1 year of follow-up in obese patients 
      with pre-diabetes treated with metformin vs. placebo.
LID - 10.1007/s00592-021-01743-5 [doi]
AB  - BACKGROUNDS: Obese pre-diabetics over express cytokines that influence myocardial 
      function via microRNAs (miRs) expression. OBJECTIVES: To evaluate 
      inflammatory/oxidative stress, miRs' expression and cardiovascular function in obese 
      pre-diabetics assigned to metformin therapy vs. placebo vs. normo-glycemics at 12 
      months of follow-up. MATERIALS AND METHODS: Eighty-three obese patients after 
      abdominoplastic surgery were divided in pre-diabetics (n 55), normo-glycemics (n 
      28), and assigned to hypocaloric diet. Pre-diabetics were assigned to metformin (n 
      23) or to placebo (n 22) plus hypocaloric diet. RESULTS: Obese pre-diabetics in 
      metformin vs. placebo, and obese pre-diabetics with placebo vs. normoglycemics, had 
      significant differences about IMT, MPI, and LVM (p < 0.05). Obese pre-diabetics in 
      metformin vs. placebo showed significant reduction in serum miR-195 and miR-27 
      (p < 0.05). Obese pre-diabetics in metformin vs. normoglycemics showed higher 
      expression of serum miR-195 and miR-27 (p < 0.05). Finally, we found inverse 
      relation between IMT and insulin, HOMA-IR, miR-195, miR-27; between LVEF and 
      Insulin, HOMA-IR, miR-195 and miR-27. We found inverse correlation between LVM and 
      sirtuin-1, Insulin, HOMA-IR, miR-195 and miR-27, and direct correlation with 
      interleukin-6. MPI inversely linked to miR-195 and miR-27. CONCLUSIONS: In obese 
      pre-diabetics', metformin significantly reduces inflammation/oxidative stress, and 
      miR-195 and miR-27, with reduction in LVM, IMT.
FAU - Sardu, Celestino
AU  - Sardu C
AUID- ORCID: 0000-0001-5099-3790
AD  - Department of Medical, Surgical, Neurological, Metabolic and Aging Sciences, 
      University of Campania "Luigi Vanvitelli", Piazza Miraglia 2, 80138, Naples, Italy. 
      drsarducele@gmail.com.
FAU - Trotta, Maria Consiglia
AU  - Trotta MC
AD  - Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, 
      Italy.
FAU - Pieretti, Gorizio
AU  - Pieretti G
AD  - Department of Plastic Surgery, University of Campania "Luigi Vanvitelli", Naples, 
      Italy.
FAU - Gatta, Gianluca
AU  - Gatta G
AD  - Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, 
      Italy.
AD  - Department of Radiology, University of Campania "Luigi Vanvitelli", Naples, Italy.
FAU - Ferraro, Giuseppe
AU  - Ferraro G
AD  - Department of Plastic Surgery, University of Campania "Luigi Vanvitelli", Naples, 
      Italy.
FAU - Nicoletti, Giovanni Francesco
AU  - Nicoletti GF
AD  - Department of Plastic Surgery, University of Campania "Luigi Vanvitelli", Naples, 
      Italy.
FAU - D' Onofrio, Nunzia
AU  - D' Onofrio N
AD  - Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, 
      Italy.
FAU - Balestrieri, Maria Luisa
AU  - Balestrieri ML
AD  - Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, 
      Italy.
FAU - D' Amico, Michele
AU  - D' Amico M
AD  - Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, 
      Italy.
FAU - Abbatecola, Angela
AU  - Abbatecola A
AD  - Department of Medical, Surgical, Neurological, Metabolic and Aging Sciences, 
      University of Campania "Luigi Vanvitelli", Piazza Miraglia 2, 80138, Naples, Italy.
FAU - Ferraraccio, Franca
AU  - Ferraraccio F
AD  - Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, 
      Italy.
FAU - Panarese, Iacopo
AU  - Panarese I
AD  - Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, 
      Italy.
FAU - Paolisso, Giuseppe
AU  - Paolisso G
AD  - Department of Medical, Surgical, Neurological, Metabolic and Aging Sciences, 
      University of Campania "Luigi Vanvitelli", Piazza Miraglia 2, 80138, Naples, Italy.
AD  - Mediterranea Cardiocentro, Naples, Italy.
FAU - Marfella, Raffaele
AU  - Marfella R
AD  - Department of Medical, Surgical, Neurological, Metabolic and Aging Sciences, 
      University of Campania "Luigi Vanvitelli", Piazza Miraglia 2, 80138, Naples, Italy.
AD  - Mediterranea Cardiocentro, Naples, Italy.
LA  - eng
PT  - Journal Article
DEP - 20210519
PL  - Germany
TA  - Acta Diabetol
JT  - Acta diabetologica
JID - 9200299
SB  - IM
OTO - NOTNLM
OT  - Inflammation
OT  - Metformin
OT  - MicroRNAs
OT  - Obesity
OT  - Oxidative stress
OT  - Pre-diabetes
EDAT- 2021/05/20 06:00
MHDA- 2021/05/20 06:00
CRDT- 2021/05/19 12:40
PHST- 2021/01/26 00:00 [received]
PHST- 2021/05/10 00:00 [accepted]
PHST- 2021/05/19 12:40 [entrez]
PHST- 2021/05/20 06:00 [pubmed]
PHST- 2021/05/20 06:00 [medline]
AID - 10.1007/s00592-021-01743-5 [pii]
AID - 10.1007/s00592-021-01743-5 [doi]
PST - aheadofprint
SO  - Acta Diabetol. 2021 May 19. doi: 10.1007/s00592-021-01743-5.

PMID- 34007244
OWN - NLM
STAT- In-Process
LR  - 20210520
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 2021
DP  - 2021
TI  - MiR-6869-5p Induces M2 Polarization by Regulating PTPRO in Gestational Diabetes 
      Mellitus.
PG  - 6696636
LID - 10.1155/2021/6696636 [doi]
LID - 6696636
AB  - The role of microRNA (miRNA) in gestational diabetes mellitus has been widely 
      investigated during the last decade. However, the altering effect of miR-6869-5p on 
      immunity and placental microenvironment in gestational diabetes mellitus is largely 
      unknown. In our study, the expression of miR-6869-5p was documented to be 
      significantly decreased in placenta-derived mononuclear macrophages, which was also 
      negatively related to PTPRO. Besides, PTPRO was negatively regulated by miR-6869-5p 
      in placenta-derived mononuclear macrophages. In vitro, miR-6869-5p inhibited 
      macrophage proliferation demonstrated by EdU and CCK-8 experiments. The inflammatory 
      response in macrophages was also significantly inhibited by miR-6869-5p, which could 
      regulate PTPRO as a target documented by luciferase reporter assay. Moreover, 
      miR-6869-5p promoted M2 macrophage polarization and thus restrain inflammation. 
      Accordingly, miR-6869-5p is involved in maintaining placental microenvironment 
      balance by preventing from inflammation and inducing M2 macrophages in gestational 
      diabetes mellitus.
CI  - Copyright © 2021 Pingping Wang et al.
FAU - Wang, Pingping
AU  - Wang P
AD  - Department of Gynecology and Obstetrics, the Affiliated Hospital of Maternal and 
      Child Health, Weifang Medical University, Weifang 261000, China.
FAU - Ma, Zhenzhi
AU  - Ma Z
AD  - Department of Pharmacy, the First Affiliated Hospital of Weifang Medical University, 
      Weifang 261000, China.
FAU - Wang, Zengyan
AU  - Wang Z
AD  - Operating Room, Zhucheng People's Hospital, Zhucheng 262200, China.
FAU - Wang, Ximei
AU  - Wang X
AD  - Department of Gynecology and Obstetrics, the Affiliated Hospital of Maternal and 
      Child Health, Weifang Medical University, Weifang 261000, China.
FAU - Zhao, Guifeng
AU  - Zhao G
AUID- ORCID: 0000-0001-8837-0142
AD  - Department of Antenatal Diagnosis, the First Affiliated Hospital of Maternal and 
      Child Health, Weifang Medical University, Weifang 261000, China.
FAU - Wang, Zengfang
AU  - Wang Z
AUID- ORCID: 0000-0002-3419-0338
AD  - Department of Gynecology and Obstetrics, the Affiliated Hospital of Maternal and 
      Child Health, Weifang Medical University, Weifang 261000, China.
LA  - eng
PT  - Journal Article
DEP - 20210430
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
SB  - IM
PMC - PMC8110425
COIS- All authors have declared no conflict of interest.
EDAT- 2021/05/20 06:00
MHDA- 2021/05/20 06:00
CRDT- 2021/05/19 06:46
PHST- 2020/12/17 00:00 [received]
PHST- 2021/03/10 00:00 [revised]
PHST- 2021/04/01 00:00 [accepted]
PHST- 2021/05/19 06:46 [entrez]
PHST- 2021/05/20 06:00 [pubmed]
PHST- 2021/05/20 06:00 [medline]
AID - 10.1155/2021/6696636 [doi]
PST - epublish
SO  - Mediators Inflamm. 2021 Apr 30;2021:6696636. doi: 10.1155/2021/6696636. eCollection 
      2021.

PMID- 34006945
OWN - NLM
STAT- In-Data-Review
LR  - 20210522
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 11
IP  - 1
DP  - 2021 May 18
TI  - In-depth transcriptomic analysis of human retina reveals molecular mechanisms 
      underlying diabetic retinopathy.
PG  - 10494
LID - 10.1038/s41598-021-88698-3 [doi]
LID - 10494
AB  - Diabetic Retinopathy (DR) is among the major global causes for vision loss. With the 
      rise in diabetes prevalence, an increase in DR incidence is expected. Current 
      understanding of both the molecular etiology and pathways involved in the initiation 
      and progression of DR is limited. Via RNA-Sequencing, we analyzed mRNA and miRNA 
      expression profiles of 80 human post-mortem retinal samples from 43 patients 
      diagnosed with various stages of DR. We found differentially expressed transcripts 
      to be predominantly associated with late stage DR and pathways such as hippo and gap 
      junction signaling. A multivariate regression model identified transcripts with 
      progressive changes throughout disease stages, which in turn displayed significant 
      overlap with sphingolipid and cGMP-PKG signaling. Combined analysis of miRNA and 
      mRNA expression further uncovered disease-relevant miRNA/mRNA associations as 
      potential mechanisms of post-transcriptional regulation. Finally, integrating human 
      retinal single cell RNA-Sequencing data revealed a continuous loss of retinal 
      ganglion cells, and Müller cell mediated changes in histidine and β-alanine 
      signaling. While previously considered primarily a vascular disease, attention in DR 
      has shifted to additional mechanisms and cell-types. Our findings offer an 
      unprecedented and unbiased insight into molecular pathways and cell-specific changes 
      in the development of DR, and provide potential avenues for future therapeutic 
      intervention.
FAU - Becker, Kolja
AU  - Becker K
AD  - Global Computational Biology & Digital Sciences, Boehringer Ingelheim Pharma GmbH & 
      Co. KG, Biberach an der Riß, Germany.
FAU - Klein, Holger
AU  - Klein H
AD  - Global Computational Biology & Digital Sciences, Boehringer Ingelheim Pharma GmbH & 
      Co. KG, Biberach an der Riß, Germany.
FAU - Simon, Eric
AU  - Simon E
AD  - Global Computational Biology & Digital Sciences, Boehringer Ingelheim Pharma GmbH & 
      Co. KG, Biberach an der Riß, Germany.
FAU - Viollet, Coralie
AU  - Viollet C
AD  - Global Computational Biology & Digital Sciences, Boehringer Ingelheim Pharma GmbH & 
      Co. KG, Biberach an der Riß, Germany.
FAU - Haslinger, Christian
AU  - Haslinger C
AD  - Global Computational Biology & Digital Sciences, Boehringer Ingelheim RCV GmbH & Co. 
      KG, Vienna, Austria.
FAU - Leparc, German
AU  - Leparc G
AD  - Translational Medicine & Clinical Pharmacology, Boehringer Ingelheim Pharma GmbH & 
      Co. KG, Biberach an der Riß, Germany.
FAU - Schultheis, Christian
AU  - Schultheis C
AD  - Translational Medicine & Clinical Pharmacology, Boehringer Ingelheim Pharma GmbH & 
      Co. KG, Biberach an der Riß, Germany.
FAU - Chong, Victor
AU  - Chong V
AD  - Therapeutic Area CNS Retinopathies Emerging Areas, BI International GmbH, Ingelheim, 
      Germany.
FAU - Kuehn, Markus H
AU  - Kuehn MH
AD  - Department of Ophthalmology and Visual Sciences, University of Iowa, Iowa City, IA, 
      USA.
AD  - Department of Veterans Affairs, Center for the Prevention and Treatment of Visual 
      Loss, Iowa City, IA, 52246, USA.
FAU - Fernandez-Albert, Francesc
AU  - Fernandez-Albert F
AD  - Global Computational Biology & Digital Sciences, Boehringer Ingelheim Pharma GmbH & 
      Co. KG, Biberach an der Riß, Germany. 
      francesc.fernandez-albert@boehringer-ingelheim.com.
FAU - Bakker, Remko A
AU  - Bakker RA
AD  - Global Department Cardio-Metabolic Diseases Research, Boehringer Ingelheim Pharma 
      GmbH & Co. KG, Biberach an der Riß, Germany. remko.bakker@boehringer-ingelheim.com.
LA  - eng
PT  - Journal Article
DEP - 20210518
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
SB  - IM
PMC - PMC8131353
COIS- KB, HK, ES, CV, GL, CS, FFA, and RAB are employed by Boehringer Ingelheim Pharma 
      GmbH & Co. KG. CH is employed by Boehringer Ingelheim RCV GmbH & Co KG. VC is 
      employed by BI International GmbH. MHK has no conflict of interest.
EDAT- 2021/05/20 06:00
MHDA- 2021/05/20 06:00
CRDT- 2021/05/19 06:29
PHST- 2021/01/22 00:00 [received]
PHST- 2021/04/15 00:00 [accepted]
PHST- 2021/05/19 06:29 [entrez]
PHST- 2021/05/20 06:00 [pubmed]
PHST- 2021/05/20 06:00 [medline]
AID - 10.1038/s41598-021-88698-3 [pii]
AID - 88698 [pii]
AID - 10.1038/s41598-021-88698-3 [doi]
PST - epublish
SO  - Sci Rep. 2021 May 18;11(1):10494. doi: 10.1038/s41598-021-88698-3.

PMID- 34006268
OWN - NLM
STAT- In-Data-Review
LR  - 20210522
IS  - 1755-8794 (Electronic)
IS  - 1755-8794 (Linking)
VI  - 14
IP  - 1
DP  - 2021 May 18
TI  - Signature RNAS and related regulatory roles in type 1 diabetes mellitus based on 
      competing endogenous RNA regulatory network analysis.
PG  - 133
LID - 10.1186/s12920-021-00931-0 [doi]
LID - 133
AB  - BACKGROUND: Our study aimed to investigate signature RNAs and their potential roles 
      in type 1 diabetes mellitus (T1DM) using a competing endogenous RNA regulatory 
      network analysis. METHODS: Expression profiles of GSE55100, deposited from 
      peripheral blood mononuclear cells of 12 T1DM patients and 10 normal controls, were 
      downloaded from the Gene Expression Omnibus to uncover differentially expressed long 
      non-coding RNAs (lncRNAs), mRNAs, and microRNAs (miRNAs). The ceRNA regulatory 
      network was constructed, then functional and pathway enrichment analysis was 
      conducted. AT1DM-related ceRNA regulatory network was established based on the Human 
      microRNA Disease Database to carry out pathway enrichment analysis. Meanwhile, the 
      T1DM-related pathways were retrieved from the Comparative Toxicogenomics Database 
      (CTD). RESULTS: In total, 847 mRNAs, 41 lncRNAs, and 38 miRNAs were significantly 
      differentially expressed. The ceRNA regulatory network consisted of 12 lncRNAs, 10 
      miRNAs, and 24 mRNAs. Two miRNAs (hsa-miR-181a and hsa-miR-1275) were screened as 
      T1DM-related miRNAs to build the T1DM-related ceRNA regulatory network, in which 
      genes were considerably enriched in seven pathways. Moreover, three overlapping 
      pathways, including the phosphatidylinositol signaling system (involving PIP4K2A, 
      INPP4A, PIP4K2C, and CALM1); dopaminergic synapse (involving CALM1 and PPP2R5C); and 
      the insulin signaling pathway (involving CBLB and CALM1) were revealed by comparing 
      with T1DM-related pathways in the CTD, which involved four lncRNAs (LINC01278, 
      TRG-AS1, MIAT, and GAS5-AS1). CONCLUSION: The identified signature RNAs may serve as 
      important regulators in the pathogenesis of T1DM.
FAU - Shi, Qinghong
AU  - Shi Q
AD  - Department of Clinical Laboratory, The Third Hospital of Jilin University, No. 126, 
      Xiantai Street, Changchun, 130033, Jilin, China.
FAU - Yao, Hanxin
AU  - Yao H
AUID- ORCID: 0000-0002-1464-2085
AD  - Department of Clinical Laboratory, The First Hospital of Jilin University, No. 1, 
      Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, China. 
      yhx0002001@jlu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20210518
TA  - BMC Med Genomics
JT  - BMC medical genomics
JID - 101319628
SB  - IM
PMC - PMC8130321
OTO - NOTNLM
OT  - CeRNAs
OT  - LncRNAs
OT  - T1DM
COIS- The authors declare no conflict of interest.
EDAT- 2021/05/20 06:00
MHDA- 2021/05/20 06:00
CRDT- 2021/05/19 05:40
PHST- 2020/08/30 00:00 [received]
PHST- 2021/03/04 00:00 [accepted]
PHST- 2021/05/19 05:40 [entrez]
PHST- 2021/05/20 06:00 [pubmed]
PHST- 2021/05/20 06:00 [medline]
AID - 10.1186/s12920-021-00931-0 [pii]
AID - 931 [pii]
AID - 10.1186/s12920-021-00931-0 [doi]
PST - epublish
SO  - BMC Med Genomics. 2021 May 18;14(1):133. doi: 10.1186/s12920-021-00931-0.

PMID- 34006140
OWN - NLM
STAT- In-Data-Review
LR  - 20210527
IS  - 1555-3892 (Electronic)
IS  - 0963-6897 (Print)
IS  - 0963-6897 (Linking)
VI  - 30
DP  - 2021 Jan-Dec
TI  - Comparison and Investigation of Exosomes Derived from Platelet-Rich Plasma Activated 
      by Different Agonists.
PG  - 9636897211017833
LID - 10.1177/09636897211017833 [doi]
LID - 09636897211017833
AB  - PRP-Exos are nanoscale cup-shaped vesicles that carry a variety of proteins, mRNAs, 
      microRNAs, and other bioactive substances. PRP-Exos can be formed through several 
      induction pathways, which determine their molecular profiles and facilitate their 
      tailormade participation in intercellular communication. Currently, little is known 
      on how the PRP-Exos activation method influences the quality and quantity of 
      PRP-Exos. The present study aims to observe and analyze the number, profile, and 
      growth factors of PRP-Exos through TEM, Nanoflow, and WB after PRP activation and 
      compare the difference in function of PRP-Exos on HUVECs, with different stimuli 
      (calcium gluconate, thrombin, or both). We found that PRP activated with both 
      thrombin and calcium gluconate harvested the highest concentration of exosomes 
      [(7.16 ± 0.46) × 10(10) particles/ml], compared to thrombin group [(4.87 ± 0.15) × 
      10(10) particles/ml], calcium gluconate group [(5.85 ± 0.43) × 10(10) particles/ml], 
      or saline group [(7.52 ± 0.19) × 10(9) particles/ml], respectively (P < 0.05) via 
      Nanoflow analysis. The WB analysis showed that cytokines (VEGF, PDGFBB, bFGF, TGF-β) 
      are differentially encapsulated in PRP-Exos, depending on the PRP stimulus, in which 
      the mixture-PRP-Exos yielded the highest concentration of cytokines. In the function 
      assay of PRP-Exos on HUVECs, the mixture-PRP-Exos promoted HUVECs proliferation, 
      increased HUVECs migration, promoted the formation of vessel-like by HUVECs via the 
      AKT ERK signal pathway more dramatically, compared with other groups. In summary, 
      our studies showed that PRP activated by the mixture of calcium gluconate and 
      thrombin harvested the best quality of exosomes which had the top biological 
      functions. This study provides a protocol for selecting appropriate PRP activators 
      to obtain high-quality exosomes for future applications.
FAU - Rui, Shunli
AU  - Rui S
AD  - The Key Laboratory of Laboratory Medical Diagnostics in the Ministry of Education 
      and Department of Clinical Biochemistry, College of Laboratory Medicine, 
      12550Chongqing Medical University, Chongqing, China.
FAU - Yuan, Yi
AU  - Yuan Y
AD  - Department of Endocrinology, Multidisciplinary Diabetic Foot Medical Center, 
      159412Chongqing Emergency Medical Center, Chongqing University Central Hospital, 
      Chongqing University, Chongqing, China.
FAU - Du, Chenzhen
AU  - Du C
AD  - Department of Endocrinology, Multidisciplinary Diabetic Foot Medical Center, 
      159412Chongqing Emergency Medical Center, Chongqing University Central Hospital, 
      Chongqing University, Chongqing, China.
FAU - Song, Peiyang
AU  - Song P
AD  - Department of Endocrinology, Multidisciplinary Diabetic Foot Medical Center, 
      159412Chongqing Emergency Medical Center, Chongqing University Central Hospital, 
      Chongqing University, Chongqing, China.
FAU - Chen, Yan
AU  - Chen Y
AD  - Department of Endocrinology, Multidisciplinary Diabetic Foot Medical Center, 
      159412Chongqing Emergency Medical Center, Chongqing University Central Hospital, 
      Chongqing University, Chongqing, China.
FAU - Wang, Hongyan
AU  - Wang H
AD  - Department of Endocrinology, Multidisciplinary Diabetic Foot Medical Center, 
      159412Chongqing Emergency Medical Center, Chongqing University Central Hospital, 
      Chongqing University, Chongqing, China.
FAU - Fan, Yahan
AU  - Fan Y
AD  - Department of Blood Transfusion, Southwest Hospital, Chongqing, China.
FAU - Armstrong, David G
AU  - Armstrong DG
AD  - Department of Surgery, Keck School of Medicine of the 12223University of Southern 
      California, CA, USA.
FAU - Deng, Wuquan
AU  - Deng W
AUID- ORCID: 0000-0002-5450-9713
AD  - Department of Endocrinology, Multidisciplinary Diabetic Foot Medical Center, 
      159412Chongqing Emergency Medical Center, Chongqing University Central Hospital, 
      Chongqing University, Chongqing, China.
FAU - Li, Ling
AU  - Li L
AD  - The Key Laboratory of Laboratory Medical Diagnostics in the Ministry of Education 
      and Department of Clinical Biochemistry, College of Laboratory Medicine, 
      12550Chongqing Medical University, Chongqing, China.
LA  - eng
PT  - Journal Article
TA  - Cell Transplant
JT  - Cell transplantation
JID - 9208854
SB  - IM
PMC - PMC8138303
OTO - NOTNLM
OT  - HUVECS
OT  - calcium gluconate
OT  - exosomes
OT  - platelet-rich plasma (PRP)
OT  - thrombin
COIS- Declaration of Conflicting Interests: The author(s) declared no potential conflicts 
      of interest with respect to the research, authorship, and/or publication of this 
      article
EDAT- 2021/05/20 06:00
MHDA- 2021/05/20 06:00
CRDT- 2021/05/19 05:34
PHST- 2021/05/19 05:34 [entrez]
PHST- 2021/05/20 06:00 [pubmed]
PHST- 2021/05/20 06:00 [medline]
AID - 10.1177_09636897211017833 [pii]
AID - 10.1177/09636897211017833 [doi]
PST - ppublish
SO  - Cell Transplant. 2021 Jan-Dec;30:9636897211017833. doi: 10.1177/09636897211017833.

PMID- 33999949
OWN - NLM
STAT- In-Data-Review
LR  - 20210528
IS  - 1553-7374 (Electronic)
IS  - 1553-7366 (Linking)
VI  - 17
IP  - 5
DP  - 2021 May
TI  - Characterization of ALTO-encoding circular RNAs expressed by Merkel cell 
      polyomavirus and trichodysplasia spinulosa polyomavirus.
PG  - e1009582
LID - 10.1371/journal.ppat.1009582 [doi]
AB  - Circular RNAs (circRNAs) are a conserved class of RNAs with diverse functions, 
      including serving as messenger RNAs that are translated into peptides. Here we 
      describe circular RNAs generated by human polyomaviruses (HPyVs), some of which 
      encode variants of the previously described alternative large T antigen open reading 
      frame (ALTO) protein. Circular ALTO RNAs (circALTOs) can be detected in virus 
      positive Merkel cell carcinoma (VP-MCC) cell lines and tumor samples. CircALTOs are 
      stable, predominantly located in the cytoplasm, and N6-methyladenosine (m6A) 
      modified. The translation of MCPyV circALTOs into ALTO protein is negatively 
      regulated by MCPyV-generated miRNAs in cultured cells. MCPyV ALTO expression 
      increases transcription from some recombinant promoters in vitro and upregulates the 
      expression of multiple genes previously implicated in MCPyV pathogenesis. MCPyV 
      circALTOs are enriched in exosomes derived from VP-MCC lines and 
      circALTO-transfected 293T cells, and purified exosomes can mediate ALTO expression 
      and transcriptional activation in MCPyV-negative cells. The related trichodysplasia 
      spinulosa polyomavirus (TSPyV) also expresses a circALTO that can be detected in 
      infected tissues and produces ALTO protein in cultured cells. Thus, human 
      polyomavirus circRNAs are expressed in human tumors and infected tissues and express 
      proteins that have the potential to modulate the infectious and tumorigenic 
      properties of these viruses.
FAU - Yang, Rong
AU  - Yang R
AD  - Department of Dermatology, UT Southwestern Medical Center, Dallas, Texas, United 
      States of America.
FAU - Lee, Eunice E
AU  - Lee EE
AD  - Department of Dermatology, UT Southwestern Medical Center, Dallas, Texas, United 
      States of America.
FAU - Kim, Jiwoong
AU  - Kim J
AUID- ORCID: 0000-0003-0220-9329
AD  - Quantitative Biomedical Research Center, Department of Population and Data Sciences, 
      UT Southwestern Medical Center, Dallas, Texas, United States of America.
FAU - Choi, Joon H
AU  - Choi JH
AD  - Department of Molecular Biosciences, University of Texas, Austin, Texas, United 
      States of America.
FAU - Kolitz, Elysha
AU  - Kolitz E
AUID- ORCID: 0000-0002-4664-2063
AD  - Department of Dermatology, UT Southwestern Medical Center, Dallas, Texas, United 
      States of America.
FAU - Chen, Yating
AU  - Chen Y
AD  - Department of Molecular Biosciences, University of Texas, Austin, Texas, United 
      States of America.
FAU - Crewe, Clair
AU  - Crewe C
AUID- ORCID: 0000-0002-3117-5327
AD  - Touchstone Diabetes Center, Department of Internal Medicine, the UT Southwestern 
      Medical Center, Dallas, Texas, United States of America.
FAU - Salisbury, Nicholas J H
AU  - Salisbury NJH
AUID- ORCID: 0000-0002-7619-6850
AD  - Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, 
      Washington, United States of America.
FAU - Scherer, Philipp E
AU  - Scherer PE
AUID- ORCID: 0000-0003-0680-3392
AD  - Touchstone Diabetes Center, Department of Internal Medicine, the UT Southwestern 
      Medical Center, Dallas, Texas, United States of America.
FAU - Cockerell, Clay
AU  - Cockerell C
AD  - Department of Dermatology, UT Southwestern Medical Center, Dallas, Texas, United 
      States of America.
FAU - Smith, Taylor R
AU  - Smith TR
AUID- ORCID: 0000-0001-8356-5987
AD  - Department of Dermatology, Louisiana State University Health Sciences Center, New 
      Orleans, Louisiana, United States of America.
FAU - Rosen, Leslie
AU  - Rosen L
AUID- ORCID: 0000-0002-8722-436X
AD  - Department of Dermatology, Louisiana State University Health Sciences Center, New 
      Orleans, Louisiana, United States of America.
FAU - Verlinden, Louisa
AU  - Verlinden L
AD  - Department of Dermatology, Ghent University Hospital, Ghent, Belgium.
FAU - Galloway, Denise A
AU  - Galloway DA
AUID- ORCID: 0000-0002-6713-6127
AD  - Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, 
      Washington, United States of America.
FAU - Buck, Christopher B
AU  - Buck CB
AUID- ORCID: 0000-0003-3165-8094
AD  - Lab of Cellular Oncology, NCI, NIH, Bethesda, Maryland, United States of America.
FAU - Feltkamp, Mariet C
AU  - Feltkamp MC
AUID- ORCID: 0000-0001-5993-9846
AD  - Department of Medical Microbiology, Leiden University Medical Center, Leiden, 
      Netherlands.
FAU - Sullivan, Christopher S
AU  - Sullivan CS
AD  - Department of Molecular Biosciences, University of Texas, Austin, Texas, United 
      States of America.
FAU - Wang, Richard C
AU  - Wang RC
AUID- ORCID: 0000-0003-4543-8295
AD  - Department of Dermatology, UT Southwestern Medical Center, Dallas, Texas, United 
      States of America.
AD  - Harold C. Simmons Cancer Center, UT Southwestern Medical Center, Dallas, Texas, 
      United States of America.
LA  - eng
PT  - Journal Article
DEP - 20210517
PL  - United States
TA  - PLoS Pathog
JT  - PLoS pathogens
JID - 101238921
SB  - IM
COIS- The authors have declared that no competing interests exist.
EDAT- 2021/05/18 06:00
MHDA- 2021/05/18 06:00
CRDT- 2021/05/17 17:29
PHST- 2021/01/05 00:00 [received]
PHST- 2021/04/24 00:00 [accepted]
PHST- 2021/05/27 00:00 [revised]
PHST- 2021/05/18 06:00 [pubmed]
PHST- 2021/05/18 06:00 [medline]
PHST- 2021/05/17 17:29 [entrez]
AID - PPATHOGENS-D-21-00027 [pii]
AID - 10.1371/journal.ppat.1009582 [doi]
PST - epublish
SO  - PLoS Pathog. 2021 May 17;17(5):e1009582. doi: 10.1371/journal.ppat.1009582. 
      eCollection 2021 May.

PMID- 33998293
OWN - NLM
STAT- Publisher
LR  - 20210518
IS  - 1522-1555 (Electronic)
IS  - 0193-1849 (Linking)
DP  - 2021 May 17
TI  - Diet-Dependent Sex Differences in the Response to Vertical Sleeve Gastrectomy.
LID - 10.1152/ajpendo.00060.2021 [doi]
AB  - Nearly 80% of patients that receive bariatric surgery are women, yet mechanistic 
      pre-clinical studies have focused on males. The goal of this study was to determine 
      the metabolic impact of diet- and surgery-induced weight loss in males, females, and 
      ovariectomized females. Male and female mice were fed a 60% high-fat (HFD) diet 
      before undergoing either vertical sleeve gastrectomy (VSG) or sham surgery. Mice 
      either remained on HFD or were switched to a standard chow diet post-surgically. 
      When maintained on HFD, both males and females decreased fat mass and improved oral 
      glucose tolerance after VSG. After dietary intervention, additional adiposity was 
      lost in both surgical groups. Ovariectomized females had a blunted decrease in fat 
      mass on a HFD, but lost significant adiposity after dietary intervention. Energy 
      expenditure was only impacted by dietary but not surgical intervention across all 
      groups. Males decreased hepatic triglyceride levels after VSG, which was further 
      decreased after dietary intervention. Intact and ovariectomized females had a 
      blunted decrease in hepatic triglycerides after surgical intervention but a 
      significant decrease after dietary intervention. The more pronounced effect of 
      surgery on hepatic lipids in males was strongly associated with changes in 
      expression of hepatic microRNAs and genes that have previously been linked to 
      hepatic lipid regulation and systemic energy homeostasis. These data highlight the 
      importance of post-surgical diet on metabolic outcomes across sexes and hormone 
      levels. Furthermore, these data suggest the impact of VSG on hepatic triglycerides 
      is diet-dependent in females and support that hypothesis that males and females 
      achieve a similar metabolic outcome, at least within the liver, via distinct 
      mechanisms.
FAU - Hutch, Chelsea R
AU  - Hutch CR
AD  - Department of Surgery, University of Michigan-Ann Arbor, United States.
FAU - Stelmak, Daria
AU  - Stelmak D
AD  - Department of Surgery, University of Michigan-Ann Arbor, United States.
FAU - Kanke, Matt
AU  - Kanke M
AD  - Department of Biomedical Sciences, College of Veterinary Medicine, Cornell 
      University, Ithaca, NY USA.
FAU - Koch-Laskowski, Kieran
AU  - Koch-Laskowski K
AD  - Department of Biomedical Sciences, College of Veterinary Medicine, Cornell 
      University, Ithaca, NY USA.
FAU - Cummings, Bethany
AU  - Cummings B
AD  - Department of Biomedical Sciences, College of Veterinary Medicine, Cornell 
      University, Ithaca, NY USA.
FAU - Griffin, Cameron
AU  - Griffin C
AD  - Department of Pediatrics, University of Michigan Medical School, Ann Arbor, MI USA.
FAU - Leix, Kyle
AU  - Leix K
AD  - Department of Surgery, University of Michigan-Ann Arbor, United States.
FAU - Sethupathy, Praveen
AU  - Sethupathy P
AD  - Department of Biomedical Sciences, College of Veterinary Medicine, Cornell 
      University, Ithaca, NY USA.
FAU - Singer, Kanakadurga
AU  - Singer K
AD  - Department of Pediatrics, University of Michigan Medical School, Ann Arbor, MI USA.
FAU - Sandoval, Darleen
AU  - Sandoval D
AD  - Department of Pediatrics, Section of Nutrition and Division of Endocrinology, 
      Metabolism and Diabetes, University of Colorado Anschutz Medical Campus, United 
      States.
LA  - eng
GR  - T32 DK101357/DK/NIDDK NIH HHS/United States
GR  - 1-18-PDF-096/American Diabetes Association Research Foundation/
GR  - 1-16-ACE-47/American Diabetes Association Research Foundation/
GR  - R01DK107282/HHS | NIH | National Institute of Diabetes and Digestive and Kidney 
      Diseases (NIDDK)/
GR  - K08DK101755/HHS | NIH | National Institute of Diabetes and Digestive and Kidney 
      Diseases (NIDDK)/
GR  - R01DK115583/HHS | NIH | National Institute of Diabetes and Digestive and Kidney 
      Diseases (NIDDK)/
GR  - R01DK121995/HHS | NIH | National Institute of Diabetes and Digestive and Kidney 
      Diseases (NIDDK)/
GR  - 1-19-IBS-252/American Diabetes Association Research Foundation/
PT  - Journal Article
DEP - 20210517
PL  - United States
TA  - Am J Physiol Endocrinol Metab
JT  - American journal of physiology. Endocrinology and metabolism
JID - 100901226
SB  - IM
OTO - NOTNLM
OT  - *bariatric surgery
OT  - *metabolism
OT  - *obesity
OT  - *sex differences
OT  - *triglycerides
EDAT- 2021/05/18 06:00
MHDA- 2021/05/18 06:00
CRDT- 2021/05/17 08:42
PHST- 2021/05/17 08:42 [entrez]
PHST- 2021/05/18 06:00 [pubmed]
PHST- 2021/05/18 06:00 [medline]
AID - 10.1152/ajpendo.00060.2021 [doi]
PST - aheadofprint
SO  - Am J Physiol Endocrinol Metab. 2021 May 17. doi: 10.1152/ajpendo.00060.2021.
