| Literature DB >> 20655308 |
Zhi-Xin Shan1, Qiu-Xiong Lin, Chun-Yu Deng, Jie-Ning Zhu, Li-Ping Mai, Ju-Li Liu, Yong-Heng Fu, Xiao-Ying Liu, Yang-Xin Li, You-Yi Zhang, Shu-Guang Lin, Xi-Yong Yu.
Abstract
Hsp60 is an important component of defense mechanisms against diabetic myocardial injury; however, the cause of Hsp60 reduction in the diabetic myocardium remains unknown. After stimulation of cardiomyocytes with high glucose in vivo and in vitro, significant up-regulation of miR-1/miR-206 and post-transcriptional modulation of Hsp 60 were observed. Serum response factor (SRF) and the MEK1/2 pathway were involved in miR-1 and miR-206 expression in cardiomyocytes. miR-1 and miR-206 regulated Hsp60 expression post-transcriptionally and accelerated cardiomyocyte apoptosis through Hsp60. These results revealed that miR-1 and miR-206 regulate Hsp60 expression, contributing to high glucose-mediated apoptosis in cardiomyocytes. Copyright 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.Entities:
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Year: 2010 PMID: 20655308 DOI: 10.1016/j.febslet.2010.07.027
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124