Zheng-Gen Jin, Ph.D.

Zheng-Gen Jin, Ph.D. Assistant Professor Zheng-Gen_Jin@urmc.rochester.edu Primary Appointment: Department of Medicine in the Aab Cardiovascular Research Institute GEBS Cluster Affiliation: CVS-Cardivascular Sciences CMM-Cellular and Molecular Basis of Medicine University of Rochester School of Medicine and Dentistry 601 Elmwood Ave, Box 679 MRBX - Rm. 2.11104 Rochester, New York 14642 Phone: (585) 273-3415 Fax: (585) 276-1914

Dr. Jin’s research has been focused on molecular regulation of vascular endothelial function. Vascular endothelial cells in blood vessels produce a number of vasodilator and vasoconstrictor substances that not only physiologically regulate vasomotor tone and vascular homeostasis, but also mediate the recruitment and activity of inflammatory cells and the propensity towards atherosclerotic lesion formation and thrombosis in the pathological condition. Normal laminar shear stress, a fractional force generated by blood flow, regulates the activity of endothelial nitric oxide synthase (eNOS) and promotes the expression of genes in endothelial cells that may protect against atherosclerosis. In contrast, oxidant stress caused by over-production of reactive oxygen species plays a major role in impairing vascular functions, by reducing the bioavailability of nitric oxide and stimulating proinflammatory pathways. By understanding the nature of molecular regulation of endothelial function and dysfunction by shear stress and oxidative stress as well as growth factors and cytokines, Dr. Jin’s research will help to develop novel therapeutic strategies for preventing atherosclerotic vascular diseases and diabetic cardiovascular complications.

The specific ongoing projects in the lab are: 1) to characterize the signaling pathways involved in flow-mediated eNOS activation and anti-inflammatory effects; 2) to identify specific intracellular signaling molecules essential for oxidative stress-induced endothelial dysfunction in diabetes; 3) to define the molecular mechanisms of angiogenesis by vascular endothelial growth factor (VEGF).

Recent Publications

1. Jin ZG *. Where is endothelial nitric oxide synthase more critical: plasma membrane or Golgi? Arterioscler Thromb Vasc Biol. 2006; 26(5): 959-61 (editorial comment).
2. Wong C and Jin ZG *. Protein kinase Calpha -dependent protein kinase D activation modulates ERK signal pathway and endothelial cell proliferation by VEGF. J Biol Chem. 2005; 280(39): 33262-9.
3. Jin ZG *, Wong C, Wu J, Berk BC. Flow shear stress stimulates Gab1 tyrosine phosphorylation to mediate Akt and eNOS activation in endothelial cells. J Biol Chem, 2005, 280(13): 12305-9.
4. Lungu AO§, Jin ZG *§, Yamawaki H, Tanimoto T, Wong C, Berk BC. Cyclosporin A inhibits flow-mediated activation of endothelial nitric oxide synthase via altering cholesterol content in caveolae. J Biol Chem. 2004 Nov; 279(47): 48794-800.
5. Narins CR, Lin DA, Burton PB, Jin ZG, Berk BC. Interleukin-18 and interleukin-18 binding protein levels before and after percutaneous coronary intervention in patients with and without recent myocardial infarction. Am J Cardiol. 2004 Nov; 94(10): 1285-7.
6. Jin ZG *, Lungu AO, Xie L, Wang M, Wong C, Berk BC. Cyclophilin A is a proinflammatory cytokine that activates endothelial cells. Arterioscler Thromb Vasc Biol. 2004 Jul; 24(7): 1186-91.
7. Jin ZG, Berk BC. SOXF: redox mediators of vascular smooth muscle cell growth. Heart. 2004 May; 90(5): 488-90 (review).
8. Jin ZG *, Ueba H, Tanimoto T, Lungu AO, Frame MD, Berk BC. Ligand-independent activation of vascular endothelial growth factor receptor 2 by fluid shear stress regulates activation of endothelial nitric oxide synthase. Circ Res. 2003 Aug; 93(4): 354-63.
9. Jin ZG, Liao DF, Chen Y and Berk BC. Identification of Secreted Oxidative Stress-Induced Factors (SOXF) and Associated Proteins: Proteomics in Vascular Biology”. In: Jennifer Van Eyk and Michael J Dunn, eds. Proteomic and Genomic Analysis of Cardiovascular Disease. Wiley-VCH Publishers, 2003; 307-316.
10. Tanimoto T, Jin ZG, Berk BC. Transactivation of vascular endothelial growth factor (VEGF) receptor Flk-1/KDR is involved in sphingosine 1-phosphate-stimulated phosphorylation of Akt and endothelial nitric-oxide synthase (eNOS). J Biol Chem. 2002 Nov; 277(45): 42997-3001.
11. Jin ZG and Berk BC. Signal transduction cascades responsive to oxidative stress in the vasculature. In: Kenneth B. Storey and Janet M. Storey, eds. Protein Adaptation and Signal Transduction. Amsterdam, Netherlands: Elsevier Science; 2001: 239-252.
12. Jin ZG, Melaragno MG, Liao DF, Yan C, Haendeler J, Suh YA, Lambeth JD, Berk BC. Cyclophilin A is a secreted growth factor induced by oxidative stress. Circ Res. 2000 Oct; 87(9): 789-96.
13. Liao DF§, Jin ZG§, Baas AS, Daum G, Gygi SP, Aebersold R, Berk BC. Purification and identification of secreted oxidative stress-induced factors from vascular smooth muscle cells. J Biol Chem. 2000 Jan; 275(1): 189-96.
* Author for correspondence. § These authors contributed equally to the work.