Angiotensin Ii Induced Human Umbilical Vein Endothelial Cells And Human Umbilical Artery Smooth Muscle Cell Integrin ¦Â <sub> 3 </ Sub> Expression

Atherosclerosis has been becoming the leading cause of morbidity and mortality all round the world. At present, it is believed that endothelium dysfunction is a key and an initial step of arteriosclerosis. The decrease of the synthesis and the release of endothelium derived relaxing factor (EDRF), accompanying with the high expression of many kinds of cell adhesion molecules is the characteristic of the dysfunction endothelium which can result in monolyte, platelets adhesion .Angiotensin II is a main peptide in renin-angiotensin system and plays an important role not only in hypertension but also in arteriosclerosis. So it is helpful to uncover its function on transcription of genes of vascular endothelial cell and vascular smooth muscle cells(VSMCs).Integrins is one branch of the cell adhesion molecular families. It can mediate cell-cell and cell-matrix interactions and its functions in atherosclerosis are becoming more and more remarkable. Integrin α_vβ3 is a member of β3 integrins. And either on the surface of endothelial cells or on the surface of vascular smooth muscle cells, integrin α_vβ3 always has critical effects on atherosclerosis. The integrin α_vβ3 on the surface of endothelial cells can induce platelets adhesion on the dysfunctionary endothelium. While on the surface of vascular smooth muscle cells, it can induce migration of VSMCs towards intima. It has been reported that the number of integrin α_vβ3 on the surface of cells was determined by the transcript level of β3 subunit gene. However, how the pathogenic factors regulate β3 subunit gene transcription in homo cells is unknown so far.In our lab, we observed high glucose, high insulin, high proinsulin and tumor necrosis factor a could adhere onto human umbilical vein endothelial cells(HUVECs) via integrin α_vβ3. And it is proved that angiotensin II increased β3 gene transcription by ELISA, RT-PCR and FISH on HUVECs . To study the mechanism of angiotensin II increasing β3 gene transcription, we repeated angiotensin II increasing β3 gene transcription by RT-PCR; With the knowledge that angiotensin II can mainly strengthen the activity of reduced form of nicotinamide-adenine dinucleotide phosphate (NADPH) at vascular wall oxidative stress produces largely subsequently as a result, we wanted to know whether antioxidant N-Acetylcysteine(NAC) and Vitamin E could inhibit angiotensin II increasing β3 gene transcription by RT-PCR or not. At the same time, we sucessfully constructed the...