Journal article
Vishalakshi Chavali, N. Tyagi, S. Tyagi, P. Mishra
2012
2012
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APA
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Chavali, V., Tyagi, N., Tyagi, S., & Mishra, P. (2012). MiR‐133 As An Epigenetic Regulator Of Diabetic Heart Failure.
Chicago/Turabian
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Chavali, Vishalakshi, N. Tyagi, S. Tyagi, and P. Mishra. “MiR‐133 As An Epigenetic Regulator Of Diabetic Heart Failure” (2012).
MLA
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Chavali, Vishalakshi, et al. MiR‐133 As An Epigenetic Regulator Of Diabetic Heart Failure. 2012.
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@article{vishalakshi2012a,
title = {MiR‐133 As An Epigenetic Regulator Of Diabetic Heart Failure},
year = {2012},
author = {Chavali, Vishalakshi and Tyagi, N. and Tyagi, S. and Mishra, P.}
}
Abstract
The miRNA has emerged as a therapeutic target for diabetic cardiomyopathy (DCM). Although epigenetic regulation of specific genes associated with DCM has been documented, the role of miRNAs in epigenetic regulation is nebulous. We tested the hypothesis that miR‐133 inhibits DNA methylation by down regulating two major genes: DNA methyltransferase (DNMT3a) and methyl‐CpG‐binding domain (MBD2) in diabetes. To prove the hypothesis, we transfected HL1 cardiomyocytes with miR‐133 and scrambled. The successful transfection was validated by GFP marker and qPCR of miR‐133 (sno234 was endogenous control). We used five treatment groups‐ a) control (CT), b) high glucose (HG‐25mM for 24 h), c) scrambled (Scr), d) miR‐133 transgenic (miR), and e) miR‐133 transgenic treated with high glucose (miR+glu) to analyze the expression of DNMT3a and MBD2 using multiplex RT‐PCR. The results revealed that DNMT3a and MBD2 are induced in HG group as compared to that of CT. However, the expression of these genes are attenuated in miR and miR+glu as compared to HG. These results suggest that high dose of glucose induces DNA methylation by up regulating DNMT3a and MBD2, whereas miR‐133 mitigates them. Our findings provide a novel insight of miR‐133 as an epigenetic regulator of DCM.
