title: β-Adrenergic Receptor-Stimulated Cardiac Myocyte Apoptosis: Role of β1 Integrins.
abstract: Increased sympathetic nerve activity to the myocardium is a central feature in patients with heart failure. Accumulation of catecholamines plays an important role in the pathogenesis of heart disease. Acting via β-adrenergic receptors (β-AR), catecholamines (norepinephrine and isoproterenol) increase cardiac myocyte apoptosis in vitro and in vivo. Specifically, β(1)-AR and β(2)-AR coupled to Gαs exert a proapoptotic action, while β(2)-AR coupled to Gi exerts an antiapoptotic action. β1 integrin signaling protects cardiac myocytes against β-AR-stimulated apoptosis in vitro and in vivo. Interaction of matrix metalloproteinase-2 (MMP-2) with β1 integrins interferes with the survival signals initiated by β1 integrins. This paper will discuss background information on β-AR and integrin signaling and summarize the role of β1 integrins in β-AR-stimulated cardiac myocyte apoptosis.
authors.affiliation: Department of Physiology, James H Quillen Veterans Affairs Medical Center, James H Quillen College of Medicine, East Tennessee State University, P.O. Box 70576, Johnson City, TN 37614, USA.
authors.forename: Parthiv
authors.initials: P
authors.lastname: Amin
authors.forename: Mahipal
authors.initials: M
authors.lastname: Singh
authors.forename: Krishna
authors.initials: K
authors.lastname: Singh