Education

B.S., Biology, Paine College, Augusta, GA, 1999
Ph.D., Biomedical Sciences, Meharry Medical College, Nashville, TN, 2005
Postdoctoral Fellow, Emory Univ. School Medicine, Dept. of Medicine, Cardiology Division, 2005-2006
FIRST Postdoctoral Fellow, Department of Cardiology, Emory University School of Medicine, 2006-2009

Research Statement

My project is based on the emerging concept that components other than angiotensin II (Ang II) are physiologically active. Recently, studies have determined that both renin and its previously believed inactive precursor prorenin can induce intracellular signaling by binding to a newly discovered renin receptor. The goals of my project are to determine if this receptor has any role in the development and progression of atherosclerosis. Currently, I am using a vascular smooth muscle cell culture model to identify the basic signaling mechanism activated by renin binding to its receptor which might lead to an atherogenic response. Our in vivo model of atherosclerosis is an apolipoprotein E knockout mouse fed a high fat diet. I am also studying the effects of pharmacological inhibition of renin and the renin receptor on blood pressure and aortic lesion formation.

Recent Publications

Woolfolk, E.A., Eguchi, S., Ohtsu, H., Nakashima, H., Ueno, H., Gerthoffer, W.T., Motley, E.D. (2005) Angiotensin II-induced activation of p21-activated kinase 1 requires Ca2+ and protein kinase C{delta} in vascular smooth muscle cells. Am J Physiol Cell Physiol. 289(5):C1286-94.

Ohtsu, H., Mifune, M., Frank, G.D., Saito, S., Inagami, T., Kim-Mitsuyama, S., Takuwa, Y., Sasaki, T., Rothstein, J.D., Suzuki, H., Nakashima, H., Woolfolk, E.A., Motley, E.D., Eguchi, S. (2005) Signal-crosstalk between Rho/ROCK and c-Jun NH2-terminal kinase mediates migration of vascular smooth muscle cells stimulated by angiotensin II. Arterioscler Thromb Vasc Biol. 25(9):1831-6.

Spelman College
Department of Biology
Atlanta, GA 30314
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