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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects*
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Apoptosis / genetics
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Apoptosis / physiology
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Base Sequence
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Chaperonin 60 / genetics
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Chaperonin 60 / metabolism*
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DNA / genetics
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DNA / metabolism
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Diabetes Mellitus, Experimental / genetics
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Diabetes Mellitus, Experimental / metabolism
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Diabetes Mellitus, Experimental / pathology
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Glucose / pharmacology*
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MAP Kinase Signaling System
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MicroRNAs / antagonists & inhibitors
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MicroRNAs / genetics*
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MicroRNAs / metabolism*
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Models, Cardiovascular
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Myocytes, Cardiac / drug effects*
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Myocytes, Cardiac / metabolism
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Myocytes, Cardiac / pathology*
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Plasmids / genetics
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RNA Processing, Post-Transcriptional
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Rats
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Rats, Sprague-Dawley
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Serum Response Factor / metabolism
Substances
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Chaperonin 60
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MIRN1 microRNA, rat
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MicroRNAs
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Serum Response Factor
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mirn206 microRNA, rat
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DNA
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Glucose