Stretch force on vascular smooth muscle cells enhances oxidation of LDL via superoxide production

被引：47

作者：

Inoue, N ^{[1
]}

Kawashima, S ^{[1
]}

Hirata, KI ^{[1
]}

Rikitake, Y ^{[1
]}

Takeshita, S ^{[1
]}

Yamochi, W ^{[1
]}

Akita, H ^{[1
]}

Yokoyama, M ^{[1
]}

机构：

[1] Kobe Univ, Sch Med, Dept Internal Med 1, Chuo Ku, Kobe, Hyogo 650, Japan

来源：

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 1998年 / 274卷 / 06期

关键词：

hemodynamic force; oxidant stress; reduced nicotinamide adenine dinucleotide reduced nicotinamide adenine dinucleotide phosphate oxidase; atherosclerosis; hypertension;

D O I：

10.1152/ajpheart.1998.274.6.H1928

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Hemodynamic forces on vasculature profoundly influence atherogenesis. mie examined the effect of stretch force on the oxidation of low-density lipoprotein (LDL) by rat aortic smooth muscle cells (RASM) and superoxide production. Stretch force was imposed on RASM cultured on deformable dishes by stretching the dishes. Incubation of native LDL with static RASM for 24 h resulted in LDL oxidation as indicated by increases in thiobarbituric acid-reacting substances from 9.5 +/- 2.3 to 24.5 +/- 2.3 nmol malondialdehyde/mg. Stretch force on RASM augmented cell-mediated LDL oxidation to 149.3 +/- 17.1% concomitantly with increase in superoxide production. LDL oxidation was inhibited by superoxide dismutase or depletion of the metal ion in the culture medium, indicating that it was a metal ion-dependent and superoxide-mediated process. The enhancement of LDL oxidation by stretch force was inhibited by diphenyliodonium, indicating the involvement of the NADH/NADPH oxidase system. Our findings suggest that the increased oxidant stress induced by stretch force is one of the potential mechanisms whereby hypertension facilitates atherosclerosis.

引用

页码：H1928 / H1932

页数：5

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