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Zheng Dong, Ph.D.
zdong@mcg.edu

Telephone: 706.721.2825
Fax: 706.721.6120
Room: CB-1124

Professor, Department of Cellular Biology and Anatomy

Departmental Director of Graduate Studies

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:

1994     Postdoctoral Fellow, Department of Pathology, UT Health Science Center

1998     Research Instructor, Department of Pathology, UT Health Science Center

1999     Assistant Professor, Department of Pathology, UT Health Science Center

2002-    Associate Professor, Department of Cellular Biology and Anatomy, MCG

2004-    Research Physiologist, Charlie Norwood VA Medical Center at Augusta, GA

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

2001   Carl W. Gottschalk Scholar Award            American Society of Nephrology

2001   Patricia W. Robinson Young Investigator    National Kidney Foundation

2004   Career Development Award                       VISN 7, VA

2005   Distinguished Faculty Award (Basic Science)     School of Medicine, MCG

2005   Distinguished Research Award                  School of Graduate Studies, MCG

2008   Career Scientist Award                             Department of Veteran Affairs

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.

 

 

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July 10, 2007