| The renin-angiotensin-aldosterone system (RAS) acts as a circulating, local endogenous tissue hormonal system with autocrine and paracrine effects. Angiotensin II (Angll), the most important octapeptide of this system, possesses most of the physiological or pathological effects of RAS. An increasing body of evidence suggests that Angll may play a major role in the pathogenesis of atherosclerosis. Angll contributes to an increase in left ventricular mass by directly promoting myocyte growth, as well as by stimulating vascular smooth muscle cell growth and proliferation. Angll has been demonstrated to lead to endothelial cell release of neutrophil chemoattractant, resulting in neutrophil accumulation. Angll induces the production and secretion of plasnimogen activator inhibitor-1 (PAI-1), endothlin-1, and adhesin molecules. Otherwise, a role for angiotensin II in apoptosis was also described. But the atherogenic mechanism of Angll has notbeen fully elucidated.Angll activates at lease 2 distinct types of cell-surface receptors, type (AT]) and type 2 (AT2). Most experimental studies have shown that it is the AT] activation mat mediates most of the known effects of Angll in the cardiovascular system. As an effective antihypertensive drug, Angll receptor antagonist (ARB) is extensively used in clinical therapy. Studies demonstrated that ARB has anti- atherogenic properties .Oxidatively modified LDL (Ox-LDL) internalized by macrophages leads to foam cell formation as a hallmark in the development of atherosclerosis. Moreover, Ox-LDL induces potentially proathrosclerotic effects in endothelial cells. The effects include impairment of endothelial NO formation, induction of endothelial expression of adhesin molecules and smooth muscle growth factors, induction of superoxide anion formation from vascular tissue, and apoptosis of endothelial cells. Ox-LDL is internalized and degraded through a scavenger receptor mediated pathway. Recently, a human endothelial receptor that mediates uptake of Ox-LDL ?Lectinlike Ox-LDL receptor-1 (LOX-1) has been cloned. This receptor is structurally distinct from scavenger receptors of macrophages and belongs to the C-type lectin family. LOX-1 is a type-II membrane protein, which can act as a cell surface endocytosis receptor for atherogenic oxidized LDL (Ox-LDL). In addition to endothelial cells, macrophages and activated vascular smooth muscle cells express LOX-1. In vivo, endothelial cells covering early atherosclerotic lesions, macrophages and smooth muscle cells accumulated in the intima of advanced atherosclerotic plaques express LOX-1. These data indicate that LOX-1 may play a major role in the pathology of atherosclerosis.The purpose of the present study was to examine the influence of Angll on expression of LOX-1. We tested whether Angll induces LOX-1 mRNA and protein expression in human umbilical vein endothelial cells (HUVECs) and THP-1 cells. Moreove, we analyzed the effect of12valsartan ,one of the ATt antagonist, on Angll induced LOX-1 expression.PartiEffects of Angiotensin II and Valsartan on Expression of Lectin-like Oxidize Low-density Lipoprotein Recepter-1 in Cultured Human Umbilical Vein Endothlial CellsAimTo evaluate the effect of angiotensin II (Angll) and a specific type I angiotensin II receptor (ATI) antagonist, valsartan, on lectin-like oxidize low-density lipoprotein recepter-1 (LOX-1) mRNA and protein expression in cultured human umbilical vein endothlial cells (HUVECs).MethodsAfter cell toxicity test of the drugs, several groups of cultured HUVECs were incubated with different drugs: (1) The HUVECs were incubated with Angll of 10"5~10'10 M for 24 hours or with 1X10"6 M Angll for various times up to 48 hours. (2) In other groups of HUVECs, valsartan (10~5?0"10 M) was added to the culture medium half an hour before cells were incubated with 10"6 M Angll for 24 hours. (3) The HUVECs were incubated with 10"6 M valsartan for 24 hours .Then HUVECs LOX-1 protein expression was measured by endothlial cell enzyme linked im...
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