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Sharon Francis-David is an Assistant Professor in the Cardiovascular Research Institute at Morehouse School of Medicine. She earned her undergraduate degree at Morgan State University and her Doctor of Philosophy degree in Physiology at University of Alabama at Birmingham. Dr. Francis-David completed postdoctoral training under the supervision of Dr. Mohan Raizada at the University of Florida in the area of hypertension before joining the Cardiovascular Research Institute in 2003.
Obesity is a major and growing health problem in the United States and throughout the world that predisposes individuals to an increased risk for developing cardiovascular diseases such as hypertension, atherosclerosis and stroke. The underlying basis for these clinical sequelae is systemic vascular disease. Expansion of adipose tissue mass during obesity alters adipocytokine, adipocyte-derived hormones, production and secretion, which can affect downstream signaling pathways that mediate changes in vascular structure and function. Serine/threonine kinases are an important class of regulatory molecules that transmit signals from adipocytokines to control rapid and reversible phosphorylation of specific substrates that influence cellular differentiation, growth and survival processes important to normal vascular function and disease development. As vascular remodeling involves changes in vascular smooth muscle cell (VSMC) migration, survival and inflammatory processes, understanding the molecular mechanisms underlying vascular proliferative diseases is a critical towards the development of effective therapeutic intervention.
The long-term research interests of the Francis-David laboratory focus on the molecular physiology and vascular biology of hypertension and obesity-related vascular diseases. In this regard, the lab identified serum and glucocorticoid-inducible kinase 1(SGK1) in aortic smooth muscle cells as a potentially important serine/threonine kinase that modulates VSMC function and vessel disease. SGK1 is a novel member of the protein kinase A, G, and C family that is regulated both transcriptionally and post-transcriptionally by a variety of signals including growth factors, glucocorticoids, hormones and cell volume. SGK1 regulates several ion and solute transport processes and its activity/expression have been linked to cardiovascular anomalies such as diabetes and hypertension. Ultimately, our research objective is to understand the role of vascular SGK1 in relevant cardiovascular diseases settings. Thus, my laboratory has the following on-going projects:
- Transcriptional and post-translational regulation of SGK1 in response to proliferative/anti-proliferative signals in vascular cells in vitro and in response to obesity and hypertension in vascular tissue in vivo
- Molecular function of SGK1 inVSMC growth and survival processes.
- Role of SGK1 in the development of obesity- and hypertension-related vascular pathophysiology
- Identification and characterization of novel SGK1 substrates
These projects rely on small rodent models of hypertension, stroke, and obesity, as well as in vitro vascular cell cultures, genomics and proteomics approaches to understand the contribution of the SGK1 signaling pathway in the progression of cardiovascular diseases.
Our work is currently supported through an NIH funded grant. Individuals interested in pursuing postdoctoral research study in the lab are encouraged to apply.
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