Ming C. Gong, MD, PhD
Associate Professor
Department of Physiology
Room 509, Wethington Building
University of Kentucky
Lexington , KY 40536-0200
Tel: (859)-323-4933 ext 81407
Fax: (859)-257-3646
e-mail: mcgong2@uky.edu
Academic Appointments:
• Department of Physiology
• Graduate Center for Nutritional Sciences
Education:
• M.D., Hunan Medical University, China
• Ph.D., Peking Union Medical College, China
Awards:
• Best Graduate of Hunan Medical University (one among seven to be awarded, from over 400 graduates)
• Postdoctoral Fellowship, American Heart Association, Virginia Affiliate (1992 to 1994)
• Career Development Award, American Diabetes Association (2004 to 2008)
• Wethington Award, University of Kentucky (2003, 2004, 2005)
• Co-Chair of the “smooth muscle” platform session, 48th and 50th American Biophysics Meeting, 02/2004
• Co-Chair of the “smooth muscle” platform session, 50th American Biophysics Meeting, 02/2006
Research:
Research in our laboratory focuses on elucidating the molecular mechanisms regulating vascular smooth muscle function under normal and diabetic conditions.
A variety of neurotransmitters, hormones and local reagents regulate vascular smooth muscle contraction and relaxation by binding to their respective specific receptors located at the plasma membrane. The force output is produced by the sliding of the myofilaments located in the cytoplasm of smooth muscle cells. One of our goals is to understand, at the molecular and cellular level, how the binding of various neurotransmitters and hormones to their receptors located at the plasma membrane activates and relays the contractile or relaxing signals to the myofilaments located in the cytoplasm. Current projects focus on the rhoA, rho-kinase and phosphatase pathway, and its interaction with the phospholipase A2 and arachidonic acid pathway.
Another major goal of our laboratory is to elucidate the molecular mechanisms responsible for vascular smooth muscle hyperreactivity under diabetic condition. Sixteen million Americans have type II diabetes, and vascular complications are the most common causes of morbidity and mortality in diabetic patients. Disturbances in vascular functionality are detected in early diabetic patients. We and others found that vascular smooth muscle tissue isolated from type II diabetic animals exhibit a significantly increased contractile response to stimuli. The molecular mechanisms that underlie such vascular smooth muscle hyperreactivity are unclear. Currently we are testing the potential causative role of up-regulated prostaglandin H synthase (PGHS, also termed COX) in the vascular smooth muscle hyperreactivity.
State-of-the-art techniques including microarray, real-time PCR, small interference RNA and adenoviral mediated gene transfer are combined with classical physiological and biochemical methods to pursue our goals.
