University of Florida
Fellowship: Hypertension and Functional Genomics
University of Alabama at Birmingham
Degree: Doctor of Philosophy in Physiology
Morgan State University
Degree: Bachelor of Science in Biology
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
The long-term research interests of the Francis laboratory focus on the molecular physiology and vascular biology of obesity and hypertension-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. Our research objective is to understand the role of vascular-derived SGK1 and its substrates in relevant cardiovascular diseases settings. In light of the emergence of a role for mitochondrial dysfunction in hypertension and obesity our research also explores the role of mitochondrial structure and function in hypertension and during obesity. Thus, my laboratory has the following on-going projects:
- Transcriptional and post-translational regulation of SGK1 in response to adipocytokines and vasoactive signals in vascular cells in vitro and in response to obesity and hypertension in vascular tissue in vivo.
- Molecular function of SGK1 in VSMC growth and mitochondrial 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 and diet-induced obesity, as well as in vitro vascular cell cultures 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.
Zhong W, Oguljahan B, Xiao Y, Nelson J, Hernandez L, Garcia-Barrio M, Francis S. “Serum and glucocorticoid-regulated kinase 1 promotes vascular smooth muscle cell
proliferation via regulation of β-catenin dynamics.” DOI: 10.1016/j.cellsig.2014.08.002
Ding G, Qin Q, He N, Francis-David SC, Hou J, Liu J, Ricks E, Yang Q. “Adiponectin and its receptors are expressed in adult cardiomyocytes and upregulated by activation of peroxisome proliferator-activated receptor gamma.” J Mol Cell Cardiol. 43: 73-84, 2007
Yang H*, Francis SC*, Sellers K, DeBarros M, Sun C, Sumners C, Katovich MJ, Ferrario C, Muro AF, Raizada MK. “Hypertension-linked decrease in brain g-adducin gene expression.” Circ Res. 91: 633-639, 2002
Honors and Awards
NIH, NHLBI Support of Competitive Research: Research Advancement Award (SC1)
Morehouse School of Medicine, Cardiovascular Research Institute P50 Co-Investigator Collaborative Award