NFATc3 is necessary for macrophage iNOS expression during myocardial ischemia and reperfusion

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American Journal of BioMedicine  Volume 2, Issue 11, pages1188-1196 November 2014

You-lin Lee; Qiong Chung;  Lei Zhang; Zhu Shen; Jie Chan


In the present study, we sought to examine whether inhibition NFATc3, improves cardiac function and reduces heart damage during IR. Hearts of male C57BL/J6 and NFATc3 knockout (KO) mice perfused by Langendorff were subjected to 25 min of global ischemia followed by 30 min reperfusion. Cardiac function was monitored throughout the perfusion period. Myocardial damage was extrapolated from LDH activity in the coronary effluent. At the end of reperfusion. Our data show that NFATc3 regulates expression of inducible nitric oxide synthase (iNOS) in macrophages stimulated after I/R. In the NFATc3 knockout (KO) mice, left ventricular developed pressure, rate pressure product, contraction and relaxation rates and coronary flow significantly improved following reperfusion compared with C57BL/J6 mice.

Keywords: Myocardial ischemia and reperfusion; NFATc3; Langendorff; macrophage iNOS

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