Oxidized Low Density Lipoproteins Induce mRNA Expression and Release of Endothelin From Human and Porcine Endothelium
作者:
Chantal Boulanger,
Felix Tanner,
Marie-Luce Béa,
Alfred Hahn,
Annick Werner,
Thomas Lüscher,
期刊:
Circulation Research
(OVID Available online 1992)
卷期:
Volume 70,
issue 6
页码: 1191-1197
ISSN:0009-7330
年代: 1992
出版商: OVID
关键词: thrombin;native low density lipoprotein;cultured endothelial cells;intact porcine aorta;dextran sulfate;phorbol esters;acetylated low density lipoprotein;cGMP
数据来源: OVID
摘要:
Experiments were designed to examine the effect of oxidized low density lipoproteins (Ox-LDLs) on the expression and the release of endothelin from cultured endothelial cells and intact blood vessels. Ox-LDLs (30–300 μg/ml), but not native low density lipoproteins (200 μg/ml), stimulated the expression of preproendothelin mRNA in porcine and human endothelial cells, leading to a time- and concentration-dependent release of the peptide into the culture medium. The Ox-LDL-stimulated release of endothelin was mimicked by acetylated low density lipoprotein and abolished by downregulation of protein kinase C by phorbol ester. In the intact porcine aorta, Ox-LDLs, but not native low density lipoproteins, also increased the release of peptide in an endothelium- and concentration-dependent manner. The maximal effect was observed at a concentration of 100 μg/ml. Incubation of the intact porcine aorta with the scavenger receptor antagonist dextran sulfate decreased the formation of endothelin evoked by Ox-LDLs. The Ox-LDL-stimulated production of the peptide was further augmented in the presence of thrombin (4 units/ml) and was unaffected by nitric oxide-generating compound 3-morpholinosydnonimine (10−5M). These results suggest that Ox-LDL may be an endogenous mediator of the augmented release of endothelin observed in hyperlipidemia and atherosclerosis. The increased production of the peptide could contribute to vasospastic events and may promote vascular smooth muscle proliferation and progression of atherosclerotic vascular disease.
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