Reactive oxygen species induce cardiomyocyte apoptosis partly through TNF-α

被引：45

作者：

Aikawa, R

Nitta-Komatsubara, Y

Kudoh, S

Takano, H

Nagai, T

Yazaki, Y

Nagai, R

Komuro, I

机构：

[1] Chiba Univ, Grad Sch Med, Dept Cardiovasc Sci & Med, Chuo Ku, Chiba 2608670, Japan

[2] Univ Tokyo, Dept Cardiovasc Med, Grad Sch Med, Tokyo, Japan

[3] Kanazawa Med Univ, Dept Cardiovasc Med, Kanazawa, Ishikawa, Japan

[4] Int Med Ctr Japan, Tokyo, Japan

来源：

CYTOKINE | 2002年 / 18卷 / 04期

关键词：

apoptosis; cardiac myocyte; H2O2; ROS; TNF-alpha;

D O I：

10.1006/cyto.2001.1007

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Many studies have indicated that oxidative stress induces apoptosis in cardiomyocytes, but its mechanism remains unknown. We examined whether tumor necrosis factor-alpha (TNF-alpha) is involved in oxidative stress-induced cardiomyocyte apoptosis. Pretreatment with anti-TNF-alpha antibody significantly decreased the number of H2O2-induced TUNEL-positive cardiomyocytes. Expression of TNF-alpha gene was upregulated by H2O2, and H2O2 mildly but significantly increased the concentration of TNF-a in the culture medium. Although neither low dose of H2O2 nor TNF-alpha induced apoptosis, stimulation with H2O2 and TNF-alpha synergistically increased apoptosis. These results suggest that oxidative stress induces apoptosis of cardiac myocytes partly through TNF-alpha. (C) 2002 Elsevier Science Ltd. All rights reserved.

引用

页码：179 / 183

页数：5

共 25 条

[1] Oxidative stress activates extracellular signal-regulated kinases through Src and ras in cultured cardiac myocytes of neonatal rats [J].