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Name:	Roy L. Sutliff
Position:	Assistant Professor of Medicine Assistant Professor of Pathology and Laboratory Medicine
Degree:	Ph.D., Medical College of Pennsylvania, 1996
Programs:	MSP, Full Member
Phone:	404 321-6111 x 7053
Address:	Atlanta VAMC, 1670 Clairmont Rd, Ste 12C-104 (Mailstop 151-P), 4900/001/1AA
Email:	rsutlif@emory.edu
Research Descriptions:
Short:	Assessment of cardiovascular pathophysiology in gene-altered mouse models.
Long:	Research in my laboratory focuses on characterizing cardiovascular pathophysiology in gene-altered mouse models. The two areas that are most heavily studied are the role of calcium regulatory proteins in regulating vascular smooth muscle/endothelium function and the cardiovascular effects of AIDS and AIDS therapeutics. Intracellular calcium levels ([Ca2+]¿) regulate numerous cellular processes including vascular smooth muscle contraction and endothelium-dependent relaxation. One of the key regulators of [Ca2+]¿ is calcium sequestration into intracellular stores by sarco(endo)plasmic reticulum Ca2+-ATPases (SERCAs). Phospholamban (PLB) is a 24-27 kDa phosphoprotein that modulates SERCA activity. Our laboratory has used a PLB "knockout" mouse model to demonstrate that PLB modulates endothelium-dependent relaxation and vascular smooth muscle contractility. Our research uses PLB knockout and transgenic models to evaluate the contribution of endothelial and vascular smooth muscle PLB to vascular contractility/relaxation and blood pressure maintenance. Using in vivo techniques such as, echocardiography and noninvasive blood pressure measurements and ex vivo techniques such as isometric force measurement in mouse vessels and Langendorff perfusions of the heart our laboratory hopes to afford a new understanding of a previously unknown pathway for the regulation of vascular-endothelial interactions. These studies underscore the physiological as well as potential pathophysiological ramifications of vascular PLB. Acquired immune deficiency syndrome (AIDS) is a global health crisis. Therapeutic agents such as AZT and protease inhibitors have been used to treat HIV-1 and have greatly increased survival of these patients. Unfortunately, with this increased survival patients are developing cardiovascular complications that result from either prolonged exposure to the HIV-1 virus or toxicity to the AIDS therapeutics. In collaboration with Dr. William Lewis, our laboratory is using noninfectious transgenic mouse models of AIDS to study the cardiovascular pathophysiology of HIV-1 proteins and AIDS therapeutics and the underlying mechanisms mediating these cardiovascular perturbations.