Relaxin is a pleiotropic hormone shown to confer cardioprotection in several preclinical models of cardiac ischemia-reperfusion injury. In the present study, the effects of up-regulating relaxin family peptide receptor 1 (RXFP1) via adeno-associated virus serotype 9 (AAV9) vectors were investigated in a mouse model of myocardial infarction. AAV9-RXFP1 vectors were generated and injected in adult male CD1 mice. Up-regulation of Rxfp1 was confirmed via quantitative polymerase chain reaction, and overexpressing animals showed increased sensitivity to relaxin-induced ventricular inotropic response. Overexpressing animals also demonstrated reduced infarct size and preserved cardiac function 24 hours after ischemia-reperfusion. Up-regulation of RXFP1 via AAV9 vectors has potential therapeutic utility in preventing adverse remodeling after myocardial infarction.
Keywords: AAV, adeno-associated virus; CMV, cytomegalovirus; GLS, global longitudinal strain; IR, ischemia-reperfusion; LV function; LV, left ventricular; MAPK, mitogen-activated protein kinase; MI, myocardial infarction; PV, pressure-volume; RXFP1; RXFP1, relaxin family peptide receptor 1; SIRO, simulated ischemia and reoxygenation; VEC, empty vector; eNOS, endothelial nitric oxide synthase; gene therapy; ischemia-reperfusion injury; mRNA, messenger ribonucleic acid; relaxin.
© 2022 The Authors.