Molecular Risk Factors of Susceptibility to Metabolic Syndrome and its Contribution to Health Disparities in Obesity, Diabetes, Cardiovascular Disease, and Cancer.
The prevalence of cardiovascular disease, diabetes, obesity, and cancer among ethnic minorities in the United States exceeds those seen in the general population. Metabolic syndrome, a group of risk factors associated with the development of cardiovascular disease and Type 2 diabetes, has reached epidemic proportions and consequently impacts public health. Our laboratory is focused on the study of metabolic syndrome as the precursor of these chronic diseases. More specifically, obesity, as one of the central pathophysiologic mechanisms underlying the syndrome that is driven by environmental stressors. Our laboratory is committed to using state-of-the-art scientific technology and approaches to determine whether obesity may constitute an earlier “upstream” target for treatment and prevention with the hope of controlling these diseases in vulnerable communities. We are looking for graduate students with a basic knowledge in molecular and genetic biology who have a genuine interest in environmental public health research to identify molecular-disease mechanisms.
Areas of Research:
• Identifying a molecular mechanism by which estrogens and endocrine disrupting chemicals promote microvascular lesion formation in pulmonary arterioles via influencing a redox sensitive transcription regulator- Inhibitor of differentiation 3 (ID3).
• Genetic association analyses between ID3 and pulmonary hypertension, metabolic syndrome, and obesity.
• Application of Bayesian modeling to predict biological pathways and networks contributing to susceptibility of metabolic syndrome by environmental stressors.
• Development of novel 3D co-culture of the human blood-brain barrier to study the effect of environmental stressors on aging.
• Identifying novel redox signaling molecules involved in the maintenance of vascular stem cells and its application to aging.
Das J.K. and Felty Q. Microvascular Lesions by Estrogen-Induced ID3: Its Implications in Cerebral and Cardiorenal Vascular Disease. J Mol Neurosci. [Epub ahead of print] (2014). doi: 10.1007/s12031-014-0401-9
Das J.K. and Felty Q. PCB153-Induced Overexpression of ID3 Contributes to the Development of Microvascular Lesions. PLoS One, 9(8):e104159. (2014). doi: 10.1371/journal.pone.0104159
Felty, Q. Proteomic 2-D DIGE profiling of human vascular endothelial cells exposed to environmentally relevant concentration of endocrine disruptor PCB153 and physiological concentration of 17β-estradiol. Cell Biol Toxicol, 27(1):49-68, (2011). doi:10.1007/s10565-010-9170-6
Felty, Q. and Porther, N. 17β-Estradiol Induced ROS via redox sensitive Id3 signaling controls the growth of human vascular endothelial cells, Atherosclerosis, 198(1), 12-21. (2008) doi:10.1016/j.atherosclerosis.2007.12.048
Felty, Q., Singh, K. P., and Roy, D. Estrogen-induced G1/S transition of G0-arrested estrogen-dependent breast cancer cells is regulated by mitochondrial oxidant signaling, Oncogene 24, 4883-4893. (2005) doi:10.1038/sj.onc.1208667