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miR‐1/miR‐206 regulate Hsp60 expression contributing to glucose‐mediated apoptosis in cardiomyocytes
Author(s) -
Shan Zhi-Xin,
Lin Qiu-Xiong,
Deng Chun-Yu,
Zhu Jie-Ning,
Mai Li-Ping,
Liu Ju-Li,
Fu Yong-Heng,
Liu Xiao-Ying,
Li Yang-Xin,
Zhang You-Yi,
Lin Shu-Guang,
Yu Xi-Yong
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.07.027
Subject(s) - hsp60 , apoptosis , microbiology and biotechnology , in vitro , heat shock protein , microrna , downregulation and upregulation , stimulation , biology , in vivo , chemistry , endocrinology , hsp70 , gene , biochemistry , genetics
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.