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

Authors: Shan, ZX  Lin, QX  Deng, CY  Zhu, JN  Mai, LP  Liu, JL  Fu, YH  Liu, XY  Li, YX  Zhang, YY  Lin, SG  Yu, XY 
Citation: Shan ZX, etal., FEBS Lett. 2010 Aug 20;584(16):3592-600. Epub 2010 Jul 24.
Pubmed: (View Article at PubMed) PMID:20655308
DOI: Full-text: 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.

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CRRD Object Information
CRRD ID: 5131625
Created: 2011-05-06
Species: All species
Last Modified: 2011-05-06
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.