Devarakonda Teja, Mauro Adolfo G, Cain Chad, Das Anindita, Salloum Fadi N
Pauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia, USA.
Department of Physiology and Biophysics, Virginia Commonwealth University, Richmond, Virginia, USA.
JACC Basic Transl Sci. 2021 Dec 22;7(1):53-63. doi: 10.1016/j.jacbts.2021.10.012. eCollection 2022 Jan.
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 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.
松弛素是一种多效性激素，在多种心脏缺血-再灌注损伤的临床前模型中显示出具有心脏保护作用。在本研究中，通过9型腺相关病毒（AAV9）载体上调松弛素家族肽受体1（RXFP1）的作用，在心肌梗死小鼠模型中进行了研究。构建了AAV9-RXFP1载体并注射到成年雄性CD1小鼠体内。通过定量聚合酶链反应证实了RXFP1的上调，过表达的动物对松弛素诱导的心室变力反应表现出更高的敏感性。过表达的动物在缺血-再灌注24小时后还表现出梗死面积减小和心脏功能保留。通过AAV9载体上调RXFP1在预防心肌梗死后不良重塑方面具有潜在的治疗效用。
