BMS 290 Human Physiology
BMS 291 Human Physiology Laboratory
Postdoctoral fellow, Cincinnati Children’s Hospital Medical Center, 2016
Ph.D., (Physiology), University of Illinois at Urbana Champaign, 2011
M.S., (Microbiology), Wuhan University, China, 2004
B.S., (Biological Sciences), Qufu Normal University, China, 2001
Heart disease is the leading cause of death worldwide. According to the data published by American Heart Association in 2015, ~610,000 people die of heart disease in the United States every year-that’s 1 in every 4 deaths. Research in my lab focuses on understanding how a group of protein phosphatases called dual specificity phosphatases (DUSPs) regulate extracellular signal-regulated kinases 1/2 (ERK1/2) signaling in the heart. Recently we have identified DUSP8 as a critical regulator of ERK1/2 activity in the heart. Knockout of Dusp8 gene in mice leads to increased ERK1/2 activity, which protects the mice from progression towards heart failure in two surgery-induced disease models. Cardiac specific overexpression of DUSP8 in mice results in decreased ERK1/2 activity, ventricular dilation, and heart failure. These data suggest that targeting DUSP8 might be a therapeutic approach for heart disease. We are currently investigating whether knockout of both DUSP6 and DUSP8, two DUSPs specific for ERK1/2, will protect the heart from disease. In this study, we propose two specific aims as follows to study the effect on ERK1/2 signaling upon loss of DUSP6 and DUSP8 proteins in the heart. Specific aim 1: generation of knockout mice with loss of both Dusp6 and Dusp8 genes. Specific aim 2: determine the effect of loss of both Dusp6 and Dusp8 genes on MAPK signaling, myocyte proliferation, and cardiac function at both rest and stimulation conditions.