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Jin Lab

Zheng-Gen Jin, Ph.D.

Associate Professor, Department of Medicine
Aab Cardiovascular Research Institute
1991 | PhD | Physiology | China - Non-Medical School
1987 | BS | Physics | China - Non-Medical School

Research Overview

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.


Jin ImageAtherosclerosis, the formation of plaque inside arterial wall, is the leading cause of death and disability in the United States and throughout the world. Atherosclerotic lesions develop in the regions of curvature, bifurcation, and branching of vessels, where fluid shear stress is low. In contrast, steady laminar flow associated with high fluid shear stress within the large straight arteries is atheroprotective.

Our research goal is to elucidate the molecular mechanisms of atherosclerosis and to identify the key molecules and signal pathways in the atheroprotective programs of laminar flow. Our recent studies have demonstrated that histone deacetylase 5 (HDAC5) plays an important role in regulation of laminar flow-sensitive genes. Current projects focus on exploring the mechanisms by which HDAC5 and other chromatin-modifying enzymes control gene transcription in vascular endothelial cells in response to laminar flow. Our studies may provide insights into the pathogenesis of atherosclerosis and lead to the development of new therapies to prevent/treat atherosclerotic disease.

Recent Publications

  1. Essential roles of Gab1 tyrosine phosphorylation in growth factor-mediated signaling and angiogenesis., Wang W, Xu S, Yin M, Jin ZG., Int J Cardiol. 2015 Feb 15;181:180-4.
  2. Histone deacetylase 5 interacts with Krüppel-like factor 2 and inhibits its transcriptional activity in endothelium., Kwon IS, Wang W, Xu S, Jin ZG., Cardiovasc Res. 2014 Oct 1;104(1):127-37.
  3. Adrenergic signaling controls RGK-dependent trafficking of cardiac voltage-gated L-type Ca2+ channels through PKD1., Jhun BS, O-Uchi J, Wang W, Ha CH, Zhao J, Kim JY, Wong C, Dirksen RT, Lopes CM, Jin ZG., Circ Res. 2012 Jan 6;110(1):59-70.
  4. Endothelial Grb2-associated binder 1 is crucial for postnatal angiogenesis., Zhao J, Wang W, Ha CH, Kim JY, Wong C, Redmond EM, Hamik A, Jain MK, Feng GS, Jin ZG.
    Arterioscler Thromb Vasc Biol. 2011 May;31(5):1016-23.
  5. PKA phosphorylates histone deacetylase 5 and prevents its nuclear export, leading to the inhibition of gene transcription and cardiomyocyte hypertrophy., Ha CH, Kim JY, Zhao J, Wang W, Jhun BS, Wong C, Jin ZG., Proc Natl Acad Sci U S A. 2010 Aug 31;107(35):15467-72.
  6. Fluid shear stress stimulates phosphorylation-dependent nuclear export of HDAC5 and mediates expression of KLF2 and eNOS., Wang W, Ha CH, Jhun BS, Wong C, Jain MK, Jin ZG., Blood. 2010 Apr 8;115(14):2971-9.

More papers: PubMed