miR-1/miR-206 regulate Hsp60 expression contributing to glucose-mediated apoptosis in cardiomyocytes

• Published in: FEBS letters Vol. 584; no. 16; pp. 3592 - 3600
• Main Authors: 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
• Format: Journal Article
• Language: English
• Published: England Elsevier B.V 20.08.2010
• Subjects: Animals; Apoptosis - drug effects; Apoptosis - genetics; Apoptosis - physiology; Base Sequence; Chaperonin 60 - genetics; Chaperonin 60 - metabolism; Diabetes Mellitus, Experimental - genetics; Diabetes Mellitus, Experimental - metabolism; Diabetes Mellitus, Experimental - pathology; DNA - genetics; DNA - metabolism; Glucose - pharmacology; H9c2 cell; High glucose; Hsp60; MAP Kinase Signaling System; MicroRNAs - antagonists & inhibitors; MicroRNAs - genetics; MicroRNAs - metabolism; miR-1; miR-206; Models, Cardiovascular; Myocytes, Cardiac - drug effects; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - pathology; Plasmids - genetics; Rats; Rats, Sprague-Dawley; RNA Processing, Post-Transcriptional; Serum Response Factor - metabolism; miR-1; Hsp60; H9c2 cell; miR-206; High glucose
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/j.febslet.2010.07.027

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.