Ischemic heart failure enhances endogenous myocardial apelin and APJ receptor expression

Cellular & Molecular Biology Letters

George P. Liao¹  Jeffrey E. Cohen¹  Kevin J. Morine¹  Vivian M. Hsu¹  William Hiesinger¹  Corinna M. Panlilio¹  Y. Joseph Woo¹  Pavan Atluri¹  Mark F. Berry¹ 

[1] Division of Cardiothoracic Surgery, Department of Surgery, University of Pennsylvania, Philadelphia, USA$$

关键词: Apelin;    G protein coupled receptor;    APJ;    Inotrope;   

DOI  :  10.2478/s11658-006-0058-7

学科分类：分子生物学，细胞生物学和基因

来源: Uniwersytet Wroclawski * Wydzial Biotechnologii / University of Wroclaw, Faculty of Biotechnology

【 摘 要 】

Apelin interacts with the APJ receptor to enhance inotropy. In heart failure, apelin-APJ coupling may provide a means of enhancing myocardial function. The alterations in apelin and APJ receptor concentrations with ischemic cardiomyopathy are poorly understood. We investigated the compensatory changes in endogenous apelin and APJ levels in the setting of ischemic cardiomyopathy. Male, Lewis rats underwent LAD ligation and progressed into heart failure over 6 weeks. Corresponding animals underwent sham thoracotomy as control. Six weeks after initial surgery, the animals underwent hemodynamic functional analysis in the presence of exogenous apelin-13 infusion and the hearts were explanted for western blot and enzyme immunoassay analysis. Western blot analysis of myocardial APJ concentration demonstrated increased APJ receptor protein levels with heart failure (1890750±133500 vs. 901600±143120 intensity units, n=8, p=0.00001). Total apelin protein levels increased with ischemic heart failure as demonstrated by enzyme immunoassay (12.0±4.6 vs. 1.0±1.2 ng/ml, n=5, p=0.006) and western blot (1579400±477733 vs. 943000±157600 intensity units, n=10, p=0.008). Infusion of apelin-13 significantly enhanced myocardial function in sham and failing hearts. We conclude that total myocardial apelin and APJ receptor levels increase in compensation for ischemic cardiomyopathy.

【 授权许可】

Unknown