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.
The specific ongoing projects in the lab are: 1) to characterize the signaling pathways involved in flow-mediated eNOS activation and anti-inflammatory effect; 2) to identify specific intracellular signaling molecules essential for oxidative stress-induced endothelial dysfunction; 3) to define the molecular mechanisms of endothelial proinflammatory and angiogenetic responses to growth factors and cytokines.
Research
Research
* Molecular regulation of vascular endothelial function.
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.
The specific ongoing projects in the lab are: 1) to characterize the signaling pathways involved in flow-mediated eNOS activation and anti-inflammatory effect; 2) to identify specific intracellular signaling molecules essential for oxidative stress-induced endothelial dysfunction; 3) to define the molecular mechanisms of endothelial proinflammatory and angiogenetic responses to growth factors and cytokines.