首页   按字顺浏览 期刊浏览 卷期浏览 Suppression of Endothelin‐1 Secretion by Lysophosphatidylcholine in Oxidized Low...
Suppression of Endothelin‐1 Secretion by Lysophosphatidylcholine in Oxidized Low Density Lipoprotein in Cultured Vascular Endothelial Cells

 

作者: Michihisa Jougasaki,   Kiyotaka Kugiyama,   Yoshihiko Saito,   Kazuwa Nakao,   Hiroo Imura,   Hirofumi Yasue,  

 

期刊: Circulation Research  (OVID Available online 1992)
卷期: Volume 71, issue 3  

页码: 614-619

 

ISSN:0009-7330

 

年代: 1992

 

出版商: OVID

 

关键词: endothelin;lipoprotein;atherosclerosis;radioimmunoassay

 

数据来源: OVID

 

摘要:

Oxidatively modified low density lipoprotein (oxidized LDL), an atherogenic lipoprotein that exists in the atherosclerotic arteries, has been shown to alter endothelial cell functions. In the present study, we examined the effects of oxidized LDL on the production of endothelin-1-like immunoreactivity (ET-1-LI) by the cultured vascular endothelial cells from porcine aorta and human umbilical vein. Incubation with oxidized LDL resulted in a dose-dependent suppression of ET-1-LI release by both endothelial cells. Oxidized LDL also inhibited thrombin-mediated stimulation of ET-1-LI secretion. However, native LDL had no effects on ET-1-LI secretion. A lipid extract from oxidized LDL, but not from native LDL, inhibited ET-1-LI secretion, indicating that the lipid component of oxidized LDL was required for the inhibition of ET-1-LI secretion. Oxidative modification of LDL was associated with degradation of a substantial amount of phosphatidylcholine to lysophosphatidylcholine (LPC). Pretreatment with defatted albumin, which is an acceptor for hydrophilic lipids including LPC, reduced LPC concentration in oxidized LDL to that in native LDL and simultaneously prevented the inhibitory effects of oxidized LDL on ET-1-LI secretion. Incubation with synthetic LPC (palmitoyl), but not with synthetic phosphatidylcholine (dipalmitoyl), suppressed ET-1-LI secretion by the endothelial cells. No cell death was observed during the incubations as judged by the trypan blue exclusion test, and protein synthesis of the endothelial cells was not affected by lipids or lipoproteins at a concentration at which suppression of ET-1-LI was observed. We concluded that LPC in oxidized LDL causes suppression of ET-1-LI release, which may counteract the vasoconstrictive properties of atherosclerotic arteries.

 

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