Articles by George Makkar in JoVE
Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function Dan Yu1,4, George Makkar2, Rajabrata Sarkar2,3,4, Dudley K. Strickland2,3,4, Thomas S. Monahan1,2,4 1Department of Surgery, Baltimore Veterans Affairs Medical Center, 2Department of Surgery, University of Maryland School of Medicine, 3Department of Physiology, University of Maryland School of Medicine, 4Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine Restenosis following cardiovascular procedures (bypass surgery, angioplasty, or stenting) is a significant problem reducing the durability of these procedures. An ideal therapy would inhibit smooth muscle cell (VSMC) proliferation while promoting regeneration of the endothelium. We describe a model for simultaneous assessment of VSMC proliferation and endothelial function in vivo.
Other articles by George Makkar on PubMed
Myristoylated Alanine-Rich Protein Kinase Substrate (MARCKS) Regulates Small GTPase Rac1 and Cdc42 Activity and Is a Critical Mediator of Vascular Smooth Muscle Cell Migration in Intimal Hyperplasia Formation Journal of the American Heart Association. Oct, 2015 | Pubmed ID: 26450120 Transcription of the myristoylated alanine-rich C kinase substrate (MARCKS) is upregulated in animal models of intimal hyperplasia. MARCKS knockdown inhibits vascular smooth muscle cell (VSMC) migration in vitro; however, the mechanism is as yet unknown. We sought to elucidate the mechanism of MARCKS-mediated motility and determine whether MARCKS knockdown reduces intimal hyperplasia formation in vivo.
MARCKS Signaling Differentially Regulates Vascular Smooth Muscle and Endothelial Cell Proliferation Through a KIS-, P27kip1- Dependent Mechanism PloS One. 2015 | Pubmed ID: 26528715 Overexpression of the myristolated alanine-rich C kinase substrate (MARCKS) occurs in vascular proliferative diseases such as restenosis after bypass surgery. MARCKS knockdown results in arrest of vascular smooth muscle cell (VSMC) proliferation with little effect on endothelial cell (EC) proliferation. We sought to identify the mechanism of differential regulation by MARCKS of VSMC and EC proliferation in vitro and in vivo.