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Faculty

Weijian Zhang, Ph.D.

Research Associate Professor, Linus Pauling Institute and Department of Biochemistry and Biophysics

Office: 359 Linus Pauling Science Center

Telephone: (541) 737-5081

Fax: (541) 737-5077

Email Address: weijian.zhang@oregonstate.edu

Mailing/Express Delivery Address:
Weijian Zhang, Ph.D.
Linus Pauling Institute
Oregon State University
307 Linus Pauling Science Center
Corvallis, OR 97331


Research Interests

Compelling evidence links oxidative stress and inflammation to major cardiovascular diseases (CVD), including atherosclerosis, hypertension, coronary heart disease, and stroke. While antioxidants and anti-inflammatories have been found to inhibit atherosclerosis in experimental animals, antioxidant vitamin trials to prevent or slow CVD in humans have been disappointing. The disparity between clinical trials and animal studies points to major gaps in our understanding of the effects and mechanisms of antioxidants in atherosclerotic vascular diseases in humans. Our long-term goal is to target oxidative stress and inflammation in humans to better understand their etiologic roles in atherosclerosis. The intracellular redox environment regulates endothelial cell function; an imbalance in this redox environment may cause upregulation of cellular adhesion molecules and pro-inflammatory and prothrombotic mediators, all of which promote atherosclerosis. We have found that lipoic acid affects redox-sensitive cellsignaling processes, transcription factors, and gene expression in endothelial and mononuclear cells, and exerts strong anti-inflammatory and anti-atherogenic effects in experimental animals. In collaboration with researchers at Oregon Health & Science University, we are currently testing whether lipoic acid supplementation reduces risk factors for the development of atherosclerosis in humans by attenuating oxidative stress and inflammation.


Education

1982 M.D., Jishou University School of Medicine, P.R. China
1987 M.S., Beijing University of Chinese Medicine & Pharmacology (BUCMP), P. R. China
1996 Ph.D., Institute of Vascular Biology and Thrombosis Research, University of Vienna, Austria

Professional Experience

1982-1984 Resident Physician, Dept. of Internal Medicine, Changsha No. 1. Hospital, China
1987-1988 Assistant of Physiology, Dept. of Physiology, BUCMP, China
1988-1992 Lecturer of Physiology, Dept. of Physiology, BUCMP, China
1996  Postdoctoral Fellow, Institute of Vascular Biology and Thrombosis Research, University of Vienna, Austria
1996-1997 Faculty Research Associate, Division of Cell Biology, The Hospital for Sick Children, the Dept. of Surgery, Toronto Hospital, University of Toronto, Canada
1997-1998 Faculty Research Associate, Institute for Gene Therapy and Molecular Medicine, The Mount Sinai Medical Center, The Mount Sinai School of Medicine, New York University, USA
1998-2001 Faculty Research Associate, Linus Pauling Institute, Oregon State University, USA
2002-2011 Assistant Professor (Sr. Res.), Linus Pauling Institute, Oregon State University
2009-2011 Assistant Professor (Sr. Res.), Department of Biochemistry and Biophysics, College of Science, Oregon State University
2011-present Associate Professor (Sr. Res.), Linus Pauling Institute, and Department of Biochemistry and Biophysics, College of Science, Oregon State University

Awards

1987 Second prize of “Excellent Scientific Research Paper”, Beijing Association of the Integration of Traditional and Western Medicine, Beijing, China
1988 Third prize of “Sun's Foundation for Medical Science Development”, The Ministry of Health, Beijing, China
1988-1990 Prize of “Excellent Scientific Research Papers”, BUCMP, Beijing, China
1992-1995 North-South Dialogue Scholarship (EH-project 894), the Austrian Academic Exchange Service, the Ministry of Education, Vienna, Austria
1994 First prize of "Highest Rated Abstract", 38th Annual Meeting of the German Society for Thrombosis and Hemostasis Research, Munich, Germany
1994 First prize of "Erwin Deutsch-Poster Award", Update in Thrombolysis Conference, Vienna, Austria

Professional Memberships

1998-present Member of the American Association for the Advancement of Science
2000-present Member of the American Heart Association

Recent Grant Support

1998-2000 NIH R01 HL56170 (Co-investigator, project 1)
2000-2005 NIH P01 HL60886 (Co-investigator, project 1)
2001-2003 NIH R03 ES11542 (Principal Investigator)
2002-2003 Pilot Project Program Grant (Principal Investigator), Linus Pauling Institute
2003-2013 NIH P01 AT002034 (Co-Project Leader, Project 1)

Recent Publications


Wei H, Zhang WJ, Leboeuf R, Frei B. (2014) Copper induces--and copper chelation by tetrathiomolybdate inhibits--endothelial activation in vitro. Redox Rep 19:40-48.

Wei H, Zhang WJ, McMillen TS, Leboeuf RC, Frei B. (2012) Copper chelation by tetrathiomolybdate inhibits vascular inflammation and atherosclerotic lesion development in apolipoprotein E-deficient mice. Atherosclerosis 223:306-313.

Zhang WJ, Wei H, Tien YT, Frei B. (2011) Genetic ablation of phagocytic NADPH oxidase in mice limits TNFalpha-induced inflammation in the lungs but not other tissues. Free Radic Biol Med 50:1517-1525.

Lotito SB, Zhang WJ, Yang CS, Crozier A, Frei B. (2011) Metabolic conversion of dietary flavonoids alters their anti-inflammatory and antioxidant properties. Free Radic Biol Med 51:454-463.

Wei H, Frei B, Beckman JS, Zhang WJ. (2011) Copper chelation by tetrathiomolybdate inhibits lipopolysaccharide-induced inflammatory responses in vivo. Am J Physiol Heart Circ Physiol 301:H712-720.

Zhang WJ, Wei H, Frei B (2010) The iron chelator, desferrioxamine, reduces inflammation and atherosclerotic lesion development in experimental mice. Exp Biol Med 235:633-641.

Zhang WJ, Wei H, Frei B (2009) Genetic deficiency of NADPH oxidase does not diminish, but rather enhances, LPS-induced acute inflammatory responses in vivo. Free Radic Biol Med 46:791-798.

Zhang WJ, Bird KE, McMillen TS, LeBoeuf RC, Hagen TM, Frei B (2008) Dietary alpha-lipoic acid supplementation inhibits atherosclerotic lesion development in apolipoprotein E-deficient and apolipoprotein E/low-density lipoprotein receptor-deficient mice. Circulation 117:421-428.

Zhang W, Wei H, Hagen T, Frei B (2007) Alpha-lipoic acid attenuates LPS-induced inflammatory responses by activating the phosphoinositide 3-kinase/Akt signaling pathway. Proc Natl Acad Sci USA 104:4077-4082.