MARCKS Signaling Differentially Regulates Vascular Smooth Muscle and Endothelial Cell Proliferation Through a p27-Dependent Mechanism

Intimal hyperplasia is the result of pathologic vascular smooth muscle cell (VSMC) dedifferentiation to a migratory and proliferative phenotype. Myristoleated alanine-rich C kinase substrate (MARCKS) is overexpressed in animal models of intimal hyperplasia. MARCKS knockdown has been demonstrated to arrest VSMC proliferation, with little effect on endothelial cell (EC) proliferation in vitro. We sought to identify the mechanism of MARCKS-mediated differential regulation of proliferation.

Source: Journal of Vascular Surgery - August 22, 2014 Category: Surgery Authors: Dan Yu, George Makkar, Tuo Dong, Dudley Strickland, Rajabrata Sarkar, Thomas S. Monahan Tags: Abstracts from the 2014 New England Society for Vascular Surgery/Eastern Vascular Society Joint Annual Meeting Source Type: research