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Zheng
Dong, Ph.D.
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Professor, Department of Cellular Biology and Anatomy Departmental Director of Graduate Studies |
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Education and Training:
1989 B.Sc.,
Microbiology, Fudan University, Shanghai, P.R. China
1994 Ph.D., Physiology, Shanghai Institute of Physiology, Chinese Academy of Sciences
1998 Postdoc University of Texas Health Science Center at San Antonio
Research Experience:
2007 Professor, Department of Cellular Biology and Anatomy, MCG
Research Career Scientist, Charlie Norwood VA Medical Center, Augusta GA
Honors and
Awards :
2000 Lyndon B.
Johnson Research Award
American Heart Association
Extramural Grant Support:
National Institutes of Health
Department of Veteran’s Affairs
Research Interest:
Our research revolves around stress responses in normal and cancer cells. We currently focus on cellular stress induced by hypoxia/ischemia and cisplatin. Hypoxia is a condition of lack of oxygen, which mimics the in vivo condition of ischemia (lack of blood supply). In normal tissues, hypoxia/ischemia is a key pathogenic factor of ischemic diseases such as stroke, myocardial infarction and acute renal failure. In cancers, hypoxia induces angiogenesis and selects therapy-resistant cells, promoting tumorigenesis. Our goal is to understand the cell injury and adaptation mechanisms of normal and cancer cells under hypoxic/ischemic stress. Cisplatin is one of the most effective and most widely used chemotherapy drugs for cancer therapy. However, during cisplatin treatment, over 25% patients experience renal injury and develop nephrotoxic renal failure. Our research is to delineate the signaling pathways underlying cisplatin-induced kidney injury and identify renal protective approaches. Our present work is mainly in the following areas:
- Mitochondrial regulation in apoptotic cell death.
- Cell signaling during hypoxia/ischemia
- Cisplatin-induced DNA damage response and cell death
- microRNA regulation in kidney diseases
Key Words:
Apoptosis; Mitochondria; Cell injury and death; DNA damage; Hypoxia; Ischemia; Cisplatin; Chemotherapy; Acute renal failure; Tumor
Techniques:
Molecular cloning; promoter analysis; Northern, Southern & Western blot; Yeast two hybrid screen, PCR, microRNA analysis, Immunoprecipitation, Immunocytochemistry; Immunofluorescence; Cell death (apoptosis/necrosis) detection.
Recent Representative Publications:
Jiang M, Wei Q, Wang J, Du Q, Yu J, Zhang L, Dong Z. Regulation of PUMA-a by p53 in Cisplatin-induced renal cell apoptosis. Oncogene 25: 4056-4066, 2006.
Wei Q, Yin X, Wang M, Dong Z. Amelioration of Ischemic Renal Injury and Renal Failure in Bid-deficient Mice. American Journal of Physiology 290: F35-F42, 2006.
Wang J, Biju M, Wang M, Haase V, Dong Z. Cytoprotective effects of hypoxia against cisplatin-induced tubular cell apoptosis: Involvement of Mitochondrial Inhibition and p53 Suppression. Journal of American Society of Nephrology 17(7):1875-1885, 2006
Wang J, Pabla N, Wang C, Wang W, Schoenlein PV, Dong Z. Caspase-mediated cleavage of ATM during cisplatin-induced tubular cell apoptosis: inactivation of its kinase activity towards p53. American Journal of Physiology, 291: F1300-F1307, 2006.
Dong Z, Saikumar P, Weinberg J, Venkatachalam M. Calcium in Cell Injury and Death. Annual Reviews of Pathology 1:405-434, 2006 (invited review).
Brooks C, Wang J, Dong Z. Characterization of Cell Clones Isolated from Hypoxia-selected Renal Proximal Tubular cells. American Journal of Physiology, 292(1):F243-52, 2007.
Jiang M, Wei Q, Pabla N, Dong G, Wang C, Yang T, Smith S, Dong Z. Effects of hydroxyl radical scavenging on cisplatin-induced p53 activation, tubular cell apoptosis and nephrotoxicity. Biochemical Pharmacology, 73(9):1499-510, 2007.
Jiang M, Pabla N, Murphy RF, Yang T, Yin XM, Degenhardt K, White E, .Dong Z. Nutlin-3 Protects Kidney Cells during Cisplatin Therapy by Suppressing Bax/Bak activation. Journal of Biological Chemistry, 282(4):2636-45, 2007.
Wei Q, Dong G, Franklin J, Dong Z. The pathological role of Bax in cisplatin nephrotoxicity. Kidney International 72(1):53-62. 2007.
Wei Q, Dong G, Yang T, Megyesi J, Price P, Dong Z. Activation and Involvement of p53 in Cisplatin-induced Nephrotoxicity. American Journal of Physiology (renal), 293:F1282-91, 2007.
Brooks C, Wei Q, Feng L, Dong G, Tao Y, Mei L, Xie Z, Dong Z. Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with Mitofusins. Proceedings of National Academy of Sciences (USA), 104: 11649-11654, 2007.
Pabla N, Dong Z. Cisplatin Nephrotoxicity: Mechanisms and Renoprotective Strategies. Kidney International, 73(9):994-1007, 2008 (invited review)
Bhatt K, Feng L, Pabla N, Liu K, Smith S, Dong Z. Effects of targeted Bcl-2 expression in mitochondria or endoplasmic reticulum on renal tubular cell apoptosis. American Journal of Physiology (renal) 294(3): F499 - F507, 2008
Dong G, Wang L, Wang C, Yang T, Kumar, Dong Z. Induction of Apoptosis in Renal Tubular Cells by Histone Deacetylase Inhibitors, a Family of Anticancer Agents. Journal of Pharmacology and Experimental Therapeutics 325(3):978-84, 2008
Periyasamy-Thandavan S, Jiang M, Wei Q, Smith R, Yin X, Dong Z. Autophagy is cytoprotective during cisplatin injury of renal proximal tubular cells. Kidney International 74, 631–640.
Jiang M, Dong Z. Regulation and Pathological Role of p53 in Cisplatin Nephrotoxicity. Journal of Pharmacology and Experimental Therapeutics 327(2):300-7, 2008 (invited review).
Pabla N, Huang S, Mi QS, Daniel R, Dong Z. ATR-Chk2 signaling in p53 activation and DNA damage response during cisplatin-induced apoptosis. Journal of Biological Chemistry 283(10): 6572 – 6583, 2008
Periyasamy-Thandavan S, Jiang M, Schoenlein P, Dong Z. Autophagy: molecular machinery, regulation and implications for renal patho-physiology. American Journal of Physiology(renal), in press (invited review), 2009
Pabla N, Murphy R, Liu K, Dong Z. The copper transporter Ctr1 contributes to cisplatin uptake by renal tubular cells during cisplatin nephrotoxicity. American Journal of Physiology (renal), 296(3):F505-11, 2009.
Jiang M, Wang C, Huang S, Yang T, Dong Z. Cisplatin-induced apoptosis in p53-deficient renal cells via the intrinsic mitochondrial pathway. American Journal of Physiology (renal), 296(5):F983-93, 2009.
Brooks C, Wei Q, Cho S, Dong Z. Regulation of Mitochondrial Dynamics in Acute Kidney Injury in Cell Culture and Rodent Models. Journal of Clinical Investigation 119(5):1275-85, 2009.