Biphasic effect of nitric oxide on the cardiac voltage-dependent anion channel

被引：26

作者：

Cheng, Qunli ^{[1
]}

Sedlic, Filip ^{[1
,2
]}

Pravdic, Danijel ^{[1
]}

Bosnjak, Zeljko J. ^{[1
,2
]}

Kwok, Wai-Meng ^{[1
,3
]}

机构：

[1] Med Coll Wisconsin, Dept Anesthesiol, Milwaukee, WI 53226 USA

[2] Med Coll Wisconsin, Dept Physiol, Milwaukee, WI 53226 USA

[3] Med Coll Wisconsin, Dept Pharmacol & Toxicol, Milwaukee, WI 53226 USA

来源：

FEBS LETTERS | 2011年 / 585卷 / 02期

关键词：

Voltage-dependent anion channel; Nitric oxide; Heart; Cardioprotection; Mitochondria; MITOCHONDRIAL PERMEABILITY TRANSITION; CYTOCHROME-C RELEASE; CELL-DEATH; REPERFUSION;

D O I：

10.1016/j.febslet.2010.12.008

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：

Nitric oxide (NO center dot) effects on the cardiac mitochondrial voltage-dependent anion channel (VDAC) are unknown. The effects of exogenous NO center dot on VDAC purified from rat hearts were investigated in this study. When incorporated into lipid bilayers, VDAC was inhibited directly by an NO center dot donor, PAPA NONOate, in a concentration-dependent biphasic manner. This was prevented by an NO center dot scavenger, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. The effect paralleled that of NO center dot in delaying the opening of the mitochondrial permeability transition (PT) pore. These biphasic effects on the cardiac VDAC and the mitochondrial PT pore reveal a tandem impact of NO center dot on the two mitochondrial entities. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：328 / 334

页数：7