Journal article
S. Nandi, Xuefei Liu, Hong Zheng, Neeru M. Sharma, Vishalakshi Chavali, K. Patel, P. Mishra
2014
2014
Semantic Scholar
DOI
Cite
Cite
APA
Click to copy
Nandi, S., Liu, X., Zheng, H., Sharma, N. M., Chavali, V., Patel, K., & Mishra, P. (2014). miR‐133a ameliorates cardiac dysfunction in diabetes: possibly by restoring β‐adrenergic receptor function and expression (1078.6).
Chicago/Turabian
Click to copy
Nandi, S., Xuefei Liu, Hong Zheng, Neeru M. Sharma, Vishalakshi Chavali, K. Patel, and P. Mishra. “MiR‐133a Ameliorates Cardiac Dysfunction in Diabetes: Possibly by Restoring β‐Adrenergic Receptor Function and Expression (1078.6)” (2014).
MLA
Click to copy
Nandi, S., et al. MiR‐133a Ameliorates Cardiac Dysfunction in Diabetes: Possibly by Restoring β‐Adrenergic Receptor Function and Expression (1078.6). 2014.
BibTeX Click to copy
@article{s2014a,
title = {miR‐133a ameliorates cardiac dysfunction in diabetes: possibly by restoring β‐adrenergic receptor function and expression (1078.6)},
year = {2014},
author = {Nandi, S. and Liu, Xuefei and Zheng, Hong and Sharma, Neeru M. and Chavali, Vishalakshi and Patel, K. and Mishra, P.}
}
Abstract
Inhibition of microRNA (miR)‐133a causes cardiac hypertrophy and fibrosis. However, the beneficial effects of miR‐133a in cardiac dysfunction remain to be examined. Furthermore, impaired contractility in diabetic hearts has been associated with attenuated expression of β1‐ and β2‐adrenergic receptors (AR). Based on these observations, we hypothesized that augmenting miR‐133a in the circulation will improve cardiac function possibly by enhancing β1‐ and β2‐AR expression in diabetic hearts. Male Sprague‐Dawley rats were injected with streptozotocin (STZ, 45mg/kg, i.v.) to induce diabetes mellitus (plasma glucose >350mg/dL). After 4 weeks these rats were treated with miR‐133a mimic or scrambled control (10^6 lentivirus, i.v.). Two weeks later the left ventricular contractility (dP/dt) were measured under basal conditions and in response to β‐AR agonist isoproterenol (0.05µg/kg, i.v). The miR‐133a treatment increased dP/dt by 25% in diabetic rats under basal condition. In addition, isoproterenol induced increase in dP/dt was significantly increased by administration of miR‐133a in diabetic rats (12618±1086 vs 9256±1103 mmHg/sec). Consistent with these observations mRNA and protein expressions of β1‐ and β2‐AR (measured by RT‐qPCR and immunoblotting) were increased in STZ+ miR‐133a as compared to STZ+ scrambled group (mRNA: β1‐AR, 2.36±0.4 fold and β2‐AR, 3.2±0.4 fold, and protein: β1‐AR, 2.52±0.01 fold and β2‐AR, 4.1±0.01 fold. These results suggest a possible novel beneficial effect of miR‐133a in improving cardiac function in diabetes.
