miR-1/miR-206 regulate Hsp60 expression contributing to glucose-mediated apoptosis in cardiomyocytes
miR-1/miR-206 regulate Hsp60 expression contributing to glucose-mediated apoptosis in cardiomyocytes
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miR-1/miR-206 调节 Hsp60 表达，促进葡萄糖介导的心肌细胞凋亡
DOI：
10.1016/j.febslet.2010.07.027
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发表时间：
2010-08-20
期刊：
影响因子：
3.5
通讯作者：
Yu, Xi-Yong
中科院分区：
文献类型：
--
作者：
Shan, Zhi-Xin;Lin, Qiu-Xiong;Yu, Xi-Yong
HSP60是糖尿病心肌损伤防御机制的重要组成部分；然而，糖尿病心肌中HSP60减少的原因尚不清楚。高糖刺激体内外心肌细胞后，miR-1/miR-206的表达显著上调，HSP60的转录后调控明显增强。血清反应因子(SRF)和MEK1/2通路参与了心肌细胞miR-1和miR-206的表达。MiR-1和miR-206在转录后调控Hsp60的表达，并通过Hsp60促进心肌细胞的凋亡。这些结果表明miR-1和miR-206调节Hsp60的表达，促进高糖诱导的心肌细胞凋亡。(C)2010年欧洲生化学会联合会。爱思唯尔出版公司版权所有。
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. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.