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Evangeline D. Motley-Johnson, Ph.D. is a Professor and the Interim Chair of the Department of Physiology, and the Associate Dean of the School of Graduate Studies and Research. She received a B.A. in Biology from University of Virginia where she worked as a laboratory research assistant in the Department of Anesthesiology at the Medical Center studying the microvasculature of normotensive verse hypertensive animals. While working in this position, Dr. Motley decided to purse graduate studies at Howard University in Washington, D.C. where she received her Ph.D. in Physiology and Biophysics. Her dissertation research was completed in the Cardiovascular Research Division at SmithKline Beecham Pharmaceuticals in King of Prussia, PA where she studied the signal transduction pathways of alpha-1 and alpha-2 receptors in the vasculature. Dr. Motley pursued her postdoctoral studies in the Department of Pharmacology and Cell Biophysics at the University of Cincinnati in Ohio where she studied sodium-calcium exchange in the vasculature. She then joined the faculty in the Department of Physiology at Meharry Medical College as an Assistant Professor, and moved through the ranks to become a tenured Professor with her current administrative positions.
Dr. Motley studies the cellular and molecular signal transduction pathways of G-protein-coupled receptors in the vascular wall of blood vessels, and how the dysfunction of these signaling pathways can contribute to cardiovascular diseases such as hypertension, atherosclerosis, and insulin resistance associated with diabetes. Dr. Motley’s lab has delineated the signaling pathway by which angiotensin II receptors cause cell proliferation, and currently, the lab is studying protease-activated receptor (PAR) signaling in endothelial cells. The lab has shown how PAR-1 and PAR-2 differentially activate endothelial nitric oxide synthase (eNOS) phosphorylation in the regulation of nitric oxide production, and current studies are delineating the role of other PARs, such as PAR-3 and PAR-4, in the signaling pathways that lead to vascular inflammation, cell migration, and proliferation in cardiovascular diseases. Understanding the signaling pathways involved in these diseases will allow therapeutic agents to be developed at the molecular level.
Dr. Motley is well published in her field of research and is a member of several National Societies such as the American Physiological Society, the American Heart Association, and the Endocrine Society. She currently serves on National Committees and review panels. She has trained ten Ph.D. graduates and has taught physiology to graduate, medical and dental students. She also has trained many high school students and undergraduates as summer research fellows.
The goal of my research is to delineate the signal transduction pathways that are involved in the development of cardiovascular diseases such as hypertension and atherosclerosis. I have studied various signaling pathways in my career starting with alpha-1 receptor signaling in the vasculature and then angiotensin II signaling. I am currently studying protease-activated receptor (PAR) signaling in endothelial cells and how it regulates endothelial nitric oxide synthase (eNOS) phosphorylation and nitric oxide (NO) production, which causes vasodilation in the vasculature. My lab has shown that PAR-1 and PAR-2 differentially activate eNOS by different signaling pathways. We have established that PAR-2 activation couples to Gq and a calcium-dependent signaling pathway to phosphorylate eNOS-Ser-1177, which leads to an increase in NO production, while PAR-1 activation couples to G12/13 and the Rho/ROCK signaling pathway to phosphorylate eNOS-Thr-495, which decreases NO production in human umbilical vein endothelial cells (HUVECs). In our current study, we hypothesize a differential coupling of PARs to the signaling pathways that regulate eNOS and NO production in primary adult human coronary artery endothelial cells (HCAECs). In this cell line, we observed that PAR-1 primarily couples to the signaling pathway that is responsible for the phosphorylation of eNOS-Ser-1177, and PAR-2 primarily couples to the the signaling pathway that is responsible for phosphorylation of eNOS-Thr-495. Our data suggests a vascular bed specific differential coupling of PARs to the signaling pathways that regulate eNOS and NO production that may be responsible for endothelial dysfunction associated with cardiovascular disease. In the future, we would like to further delineate the roles of PAR-3 and PAR-4 in the signaling pathways that lead to vascular inflammation, cell migration and proliferation in cardiovascular diseases.
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