Journal article
P. Mishra, O. Awe, Naira S. Metreveli, Natia Qipshidze, C. Munjal, N. Tyagi, S. Tyagi
2011
2011
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APA
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Mishra, P., Awe, O., Metreveli, N. S., Qipshidze, N., Munjal, C., Tyagi, N., & Tyagi, S. (2011). Exercise ameliorates diabetic cardiomyopathy by inducing beta2‐adrenergic receptors and miR‐133a, and attenuating MMP‐9.
Chicago/Turabian
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Mishra, P., O. Awe, Naira S. Metreveli, Natia Qipshidze, C. Munjal, N. Tyagi, and S. Tyagi. “Exercise Ameliorates Diabetic Cardiomyopathy by Inducing beta2‐Adrenergic Receptors and MiR‐133a, and Attenuating MMP‐9” (2011).
MLA
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Mishra, P., et al. Exercise Ameliorates Diabetic Cardiomyopathy by Inducing beta2‐Adrenergic Receptors and MiR‐133a, and Attenuating MMP‐9. 2011.
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@article{p2011a,
title = {Exercise ameliorates diabetic cardiomyopathy by inducing beta2‐adrenergic receptors and miR‐133a, and attenuating MMP‐9},
year = {2011},
author = {Mishra, P. and Awe, O. and Metreveli, Naira S. and Qipshidze, Natia and Munjal, C. and Tyagi, N. and Tyagi, S.}
}
Abstract
To test the hypothesis that exercise ameliorates diabetic cardiomyopathy by inducing beta2‐adrenergic receptors (AR) and microRNA‐133a (miR‐133a), and attenuating matrix metalloproteinase‐9 (MMP‐9); ten weeks male db/db (a model for T2D)‐ DB (i) mice were treated with salbutamol (a beta2‐AR agonist‐200μg/kg/i.p)‐DBS (ii), exercised (swimming‐1hr/daily)‐DBE (iii), and both treated with salbutamol and exercised (DBES) (iv) for ten days. The cardiac function was determined by echocardiography and contractile function of cardiomyocytes. The levels of beta2‐adrenergic receptors (AR), miR‐133a and MMP‐9 were measured by Western blot, RT‐PCR and qPCR. The results show decrease in percentage fractional shortening (%FS=~30) in db/db mice. The improvement in contractile function (±dL/dt) of cardiomyocytes was evident from significant decrease in the time (sec) to attain 90% peak height in DBE (0.175±0.004) and DBES (0.168±0.002) as compared to DB (0.178±0.002) cardiomyocytes, and corroborated by calcium consumption ratio during the same duration DBE (19.02±1.09), DBES (24.13±1.69), and DB (15.46±0.80). The beta2‐AR and miR‐133a were up regulated, and MMP‐9 was down regulated in DBS, DBE and DBES heart as compared to DB group. Based on these findings, we conclude that exercise ameliorates cardiac dysfunction in db/db mice by improving beta2‐AR response and miR‐133a, and attenuating MMP‐9.
