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

FEBS Lett. 2010 Aug 20;584(16):3592-600. doi: 10.1016/j.febslet.2010.07.027. Epub 2010 Jul 24.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / genetics
  • Apoptosis / physiology
  • Base Sequence
  • Chaperonin 60 / genetics
  • Chaperonin 60 / metabolism*
  • DNA / genetics
  • DNA / metabolism
  • Diabetes Mellitus, Experimental / genetics
  • Diabetes Mellitus, Experimental / metabolism
  • Diabetes Mellitus, Experimental / pathology
  • Glucose / pharmacology*
  • MAP Kinase Signaling System
  • MicroRNAs / antagonists & inhibitors
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism*
  • Models, Cardiovascular
  • Myocytes, Cardiac / drug effects*
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology*
  • Plasmids / genetics
  • RNA Processing, Post-Transcriptional
  • Rats
  • Rats, Sprague-Dawley
  • Serum Response Factor / metabolism

Substances

  • Chaperonin 60
  • MIRN1 microRNA, rat
  • MicroRNAs
  • Serum Response Factor
  • mirn206 microRNA, rat
  • DNA
  • Glucose