Tsui-Chun Tsou, Ph.D.
Division of Environmental Health and Occupational Medicine
EDUCATIONPh.D., Department of Life Sciences, National Tsing Hua University
B.S., Department of Oceanography, Division of Marine Biology, Chinese Culture University
PROFESSIONAL EXPERIENCES- Associate Investigator, Division of Environmental Health and Occupational Medicine, National Health Research Institutes (2006 - present)
- Assistant Investigator, Division of Environmental Health and Occupational Medicine, National Health Research Institutes (2000 - 2006)
- Postdoctoral Fellow, Cellular and Vascular Mechanics Laboratory, Department of Bioengineering, University of California, San Diego (1997-2000)
- Postdoctoral Fellow, Molecular Carcinogenesis Laboratory, Department of Life Sciences, National Tsing Hua University (1996-1997)
RESEARCH INTERESTSThe focus of the group is the investigation of molecular mechanisms of responses to environmental toxicants involved in the etiology and progression of injury and disease processes. Cellular responses to environmental toxicants and stressors have profound implications for diverse aspects of human health and disease. Understanding the mechanisms underlying health impacts provides insights that are necessary for the development of therapeutic strategies to prevent disease. Recently, Dr. Tsou’s team mainly focuses on investigation of (1) environmental risk factors for vascular dysfunction, (2) environmental obesogens for metabolic syndrome, and (3) Environmental carcinogenesis.
RESEARCH ACTIVITIES & ACCOMPLISHMENTSDr. Tsou has been studying the effects of environmental stress on the functions of vascular system since 1997. The topics of his studies include the effects of mechanical stretch on vascular smooth muscle cells, the effects of shear stress on vascular endothelial cells, and recently the effects of arsenic exposure on vascular endothelial dysfunction. Currently, Dr. Tsou’s team is mainly focusing on investigating the arsenic effects on vascular endothelial dysfunction, the earliest changes that precede the formation of atherosclerotic lesions. They showed that arsenite affected intracellular glutathione/redox status as well as NF-?B and AP-1 activities in vascular endothelial cells. They revealed that arsenite enhanced the TNF-?-induced adhesion expression via regulation of AP-1 and NF-?B activities in a glutathione-sensitive manner and demonstrated that arsenite induced cytotoxicity by down-regulation of vascular endothelial nitric oxide synthase in vascular endothelial cells. The objective of their recent study is to explore the molecular mechanism by which environmental risk factors affect metabolism dysregulation of adipocytes via interaction with nuclear receptors. They will establish an array of nuclear receptor/nuclear receptor responsive element-driven chemical-activated luciferase expression systems (NR/NRRE CALUX) to evaluate the activation or inhibition of nuclear receptors by environmental pollutants. Then, the environmental pollutants with higher potency in modulation of nuclear receptor activity will be selected to evaluate their roles in regulating adipogenesis, fat metabolism (lipogenesis and lipolysis), and expression of adipokines (a group of cytokines secreted by adipose tissue).
SELECTED PUBLICATIONS1. Chao HR, Wang YF, Chen HT, Ko YC, Chang EE, Huang YJ, Tsai FY, Tsai CH, Wu CH, Tsou TC*. Differential effect of arecoline on the endogenous dioxin-responsive cytochrome P450 1A1 and on a stably transfected dioxin-responsive element-driven reporter in human hepatoma cells. Journal of Hazardous Materials, 149:234–237, 2007.
2. Tsou TC*, Yeh SC, Tsai FY, Chen JW, and Chiang HC. Glutathione regulation of redox-sensitive signals in tumor necrosis factor-α-induced vascular endothelial dysfunction. Toxicology and Applied Pharmacology, 221:168-178, 2007.
3. Chang EE, Miao ZF, Lee WJ, Chao HR, Li LA, Wang YF, Ko YC, Tsai FY, Yeh SC, Tsou TC*. Arecoline inhibits the 2,3,7,8-tetrachlorodibenzo-p-dioxin -induced cytochrome P450 1A1 activation in human hepatoma cells. Journal of Hazardous Materials, 146:356-361, 2007.
4. Tsou TC*, Tsai FY, Yeh SC, Chang LW. ATM/ATR-related checkpoint signals mediate arsenite-induced G2/M arrest in primary aortic endothelial cells. Archives of Toxicology, 80:804-810, 2006.
5. Chao HR, Tsou TC*, Li LA, Tsai FY, Wang YF, Tsai CH, Chang EE, Miao ZF, Wu CH, Lee WJ. Arsenic inhibits induction of cytochrome P450 1A1 by 2,3,7,8-tetrachloronated dibenzo-p-dioxin in human hepatoma cells. Journal of Hazardous Materials, 137:716-722, 2006.
6. Cheng Y, Chang LW, Tsou TC*. Mitogen-activated protein kinases mediate arsenic-induced down-regulation of survivin in human lung adenocarcinoma cells. Archives of Toxicology, 80:310-318, 2006.
7. Tsou TC*, Tsai FY, Hsieh YW, Li LA, Yeh SC, Chang LW. Arsenite induces endothelial cytotoxicity by down-regulation of vascular endothelial nitric oxide synthase. Toxicology and Applied Pharmacology, 208:277-284, 2005.
8. Tsou, TC*, Yeh SC, Tsai EM, Tsai FY, Chao HR, Chang LW. Arsenite enhances tumor necrosis factor-α-induced expression of vascular cell adhesion molecule-1. Toxicology and Applied Pharmacology, 209:10-18, 2005.
9. Tsou TC*, Yeh SC, Tsai FY, Chang LW. The protective role of intracellular glutathione status in the arsenite-induced vascular endothelial dysfunction. Chemical Research in Toxicology, 17:208-217, 2004.
10. Tsou TC*, Tsai FY, Wu MC, Chang LW. The protective role of NF-kB and AP-1 in arsenite-induced apoptosis in aortic endothelial cells. Toxicology and Applied Pharmacology, 191:177-187, 2003.