West Virginia University, Ph.D., 2005
There are two research directions in my laboratory: 1) investigating the mechanism and potential intervention strategies for ethanol neurotoxicity targeting the Fetal Alcohol Spectrum Disorders (FASD); and 2) to examine the mechanism and possible therapeutic targets for environmental factors, such as heavy metals induced cancers.
FASD is a range of permanent birth defects caused by maternal alcohol consumption during pregnancy. It is a severe public health problem. The ultimate goal for this research is to find strategies for the prevention and treatment of FASD. Our overall approach is first to determine the molecular mechanism(s) underlying ethanol-induced neuronal loss which is the most deleterious effects of fetal alcohol exposure. Then we will identify the responsible targets (genes, proteins or signaling pathways) using pharmacological or genetic manipulation methods. Finally, we will determine whether ethanol-induced neuronal loss is ameliorated by regulating the targets in animals and whether ethanol-induced behavioral deficits are improved by analyzing the behavior of the animals.
Some heavy metals (e.g. arsenic and chromium) are carcinogens; chronic exposure to these metals may cause cancer. Kentucky has a high age-adjusted lung cancer incidence rate in the nation and the concentrations of arsenic in the well water and soil in many areas far exceed the maximum contamination level (CML) set by the U.S. Environmental Protection Agency. One of my research interests is to investigate the mechanism of environment factors-induced carcinogenesis.
1. Gang Chen; Zunji Ke; Mei Xu; Mingjun Liao; Xin Wang; Yuanlin Qi, Tao Zhang, Jacqueline A. Frank ; Kimberly A. Bower; Xianglin Shi; Jia Luo. Autophagy is a Protective Response to Ethanol Neurotoxicity. Autophagy. 2012 Nov 1:8(11).
2. Tao Zhang; Yuanlin Qi; Mingjun Liao; Mei Xu; Kimberley A. Bower; Jacqueline A. Frank ; Han-Ming Shen; Jia Luo; Xianglin Shi, Gang Chen. Autophagy is a cell self-protective mechanism against arsenic-induced cell transformation. Toxicol Sci. 2012 Aug 5.
3. Gang Chen, Jia Luo. Anthocyanins: are they beneficial in treating ethanol neurotoxicity? Neurotox Res. 2010 Jan;17(1):91-101
4. Gang Chen, Kimberly A. Bower, Mei Xu, Min Ding, Xianglin Shi, Zun-Ji Ke and Jia Luo. Cyanidin-3-glucoside reverses ethanol-induced inhibition of neurite outgrowth: role of glycogen synthase kinase 3 beta. Neurotox Res. 2009 May; 15(4):321-31.
5. Gang Chen, Cuiling Ma, Kimberly A. Bower, XiangLin Shi, Zunji Ke, Jia Luo. Ethanol promotes ER stress-induced neuronal death via induction of intracellular ROS levels. J Neurosci Res. 2008 Mar;86(4):937-46.
6. Gang Chen, Zhiqin Fan, Xin Wang, Cuiling Ma, Kimberly A. Bower, Xianglin Shi, Zun-Ji Ke, and Jia Luo. Brain-derived neurotrophic factor suppresses tunicamycin-induced up-regulation of CHOP in neurons. J Neurosci Res. 2007 Jun;85(8):1674-84.