alexa Preservation of Cardiac Function and Attenuation of Remodelling in Transient Receptor Potential Vanilloid 4 Knockout Mice Following Myocardial Infarctionnd Medical Center
ISSN: 2155-9880

Journal of Clinical & Experimental Cardiology
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Research Article

Preservation of Cardiac Function and Attenuation of Remodelling in Transient Receptor Potential Vanilloid 4 Knockout Mice Following Myocardial Infarctionnd Medical Center

Gregory H Turner1, Weike Bao2*, Beat M Jucker2, John J Lepore2, Robert N Willette2, and Kevin S Thorneloe2
1BNI-ASU Center for Preclinical Imaging, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, USA
2Heart Failure Discovery Performance Unit, Metabolic Pathways and Cardiovascular Unit, GlaxoSmithKline Pharmaceuticals, King of Prussia, PA, USA
Corresponding Author : Bao W
Heart Failure Discovery Performance Unit
Metabolic Pathways and Cardiovascular Unit
GlaxoSmithKline Pharmaceuticals
King of Prussia, PA-19406, USA
Tel: 6109522564
E-mail: [email protected]
Received February 17, 2015; Accepted March 18, 2015; Published March 28, 2015
Citation: Turner GH, Bao W, Jucker BM, Lepore JJ, Willette RN et al. (2015) Preservation of Cardiac Function and Attenuation of Remodelling in Transient Receptor Potential Vanilloid 4 Knockout Mice Following Myocardial Infarction. J Clin Exp Cardiolog 6:366. doi:10.4172/2155-9880.1000366
Copyright: © 2015 Turner GH. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Transient receptor potential channel vanilloid 4 (TRPV4) is a non-selective Ca2+ permeable cation channel, recently implicated by computational methods as a key signalling component during myocardial infarction. We previously showed that pharmacological TRPV4 inhibition can prevent and resolve pulmonary edema in pre-clinical heart failure animal models. Here, we examined the impact of genetic deletion of TRPV4 (TRPV4-/-) on cardiac function, both basally and following myocardial infarction. Cardiac function was similar in wild type and TRPV4-/- mice under normal conditions. By contrast, following myocardial infarction induced by permanent ligation of the left anterior descending coronary artery, left ventricular systolic and diastolic volumes were reduced and ejection fraction was significantly improved in TRPV4-/- when compared to wild type mice. Consistent with the differences in chamber volumes between TRPV4-/- and wild type mice, myocardial infarction induced a significant increase in heart weight and left ventricular mass index in wild type, but not in TRPV4-/- mice. In a separate cohort of mice, we also investigated the effect of genetic deletion of TRPV4 on infarct size after a 30 min myocardial ischemia and 24 hours reperfusion. There were no differences in myocardial infarct size or area at risk in TRPV4-/- and wild type mice after ischemia/reperfusion injury. These results suggest that TRPV4 does not mediate acute myocardial ischemic injury, but does play an important role in ventricular remodelling known to correlate with poor outcomes following acute myocardial infarction.

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