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miR-483-3p regulates hyperglycaemia-induced cardiomyocyte apoptosis in transgenic mice.

Abstract
Diabetic cardiomyopathy represents severe heart complications, and is the leading cause of morbidity and mortality among patients with diabetes. Although a few microRNAs (miRNAs) have been implicated in diabetes-related complications, a functional association between miRNAs and cardiac dysfunction in diabetic cardiomyopathy remains to be demonstrated. Our results show that miR-483-3p is upregulated in streptozotocin-induced diabetic mice, and cultured cardiomyocytes mimicking hyperglycemia. Overexpressing miR-483-3p in transgenic mice with diabetes mellitus (DM) exacerbated cardiomyocyte apoptosis by transcriptionally repressing insulin growth factor 1 (IGF1). Therefore, we have uncovered a novel signaling pathway, involving miR-483-3p-IGF1, that promotes myocardial cell apoptosis under high blood-glucose condition. Further, our study indicates that miR-483-3p could be a potential therapeutic target for managing diabetes-associated heart complications.
AuthorsYu Qiao, Yanli Zhao, Yan Liu, Ning Ma, Chuxuan Wang, Jiaqi Zou, Zhiyan Liu, Zhongqiu Zhou, Dong Han, Jun He, Qian Sun, Yicong Liu, Changqing Xu, Zhimin Du, Hui Huang
JournalBiochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 477 Issue 4 Pg. 541-547 (09 02 2016) ISSN: 1090-2104 [Electronic] United States
PMID27346130 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2016 Elsevier Inc. All rights reserved.
Chemical References
  • MicroRNAs
  • Mirn483 microRNA, mouse
  • Streptozocin
Topics
  • Animals
  • Apoptosis (genetics)
  • Cell Line
  • Diabetes Mellitus, Experimental (genetics)
  • Hyperglycemia (genetics)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • MicroRNAs (genetics)
  • Myocytes, Cardiac (pathology)
  • Rats
  • Streptozocin

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