Gregory Turner1, Weike Bao, Beat Jucker, Kevin Thorneloe, Robert Willette
1GlaxoSmithKline, King of Prussia, PA, USA
The Transient Receptor Potential V4 (TRPV4), expressed in endothelium throughout the cardiovascular system, is a cation channel that contributes to intracellular Ca++ homeostasis and cell volume regulation . Pharmacologic activation of TRPV4 has been associated with circulatory collapse and failure of the endothelial barrier. In the present study, the effects of TRPV4 deletion (TRPV4-/-) on cardiac function was examined in a myocardial infarction (MI) model. MRI revealed preservation of cardiac function in the TRPV4-/- mouse 1 week post-MI. These results indicate that TRPV4 deletion produces a cardio-protective phenotype and suggests an important relationship between the endothelium and cardiac function.