Brain mitochondrial uncoupling protein 2 (UCP2): a protective stress signal in neuronal injury

被引：102

作者：

Bechmann, I

Diano, S

Warden, CH

Bartfai, T

Nitsch, R

Horvath, TL

机构：

[1] Yale Univ, Sch Med, Dept Obstet & Gynecol, New Haven, CT 06520 USA

[2] Humboldt Univ, Charite, Dept Anat & Cell Biol, Berlin, Germany

[3] Univ Calif Davis, Dept Pediat, Davis, CA 95616 USA

[4] Scripps Res Inst, Dept Neuropharmacol, La Jolla, CA USA

[5] Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06520 USA

来源：

BIOCHEMICAL PHARMACOLOGY | 2002年 / 64卷 / 03期

关键词：

mitochondrial uncoupling proteins; brain injury; neuronal degeneration; microglia; hippocampus;

D O I：

10.1016/S0006-2952(02)01166-8

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Mitochondrial uncoupling proteins (UCPs) can dissociate oxidative phosphorylation from respiration, and they appear to be critical for energy balance. One of these proteins, UCP2, is also expressed in neurons of subcortical brain regions of healthy subjects. Here, we report on the protective role of UCP2 in brain injury by revealing its early induction after lesions and its inverse relationship with activation of an apoptotic signal, caspase 3, in wild-type and UCP2 overexpressing transgenic mice. (C) 2002 Elsevier Science Inc. All rights reserved.

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页码：363 / 367

页数：5

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