Identification of thioredoxin-2 as a regulator of the mitochondrial permeability transition

被引：38

作者：

He, Min ^{[1
,2
]}

Cai, Jiyang ^{[3
]}

Go, Young-Mi ^{[1
]}

Johnson, Jennifer M. ^{[1
,2
]}

Martin, W. David ^{[4
]}

Hansen, Jason M. ^{[5
]}

Jones, Dean P. ^{[1
]}

机构：

[1] Emory Univ, Dept Med, Div Pulm Allergy & Crit Care Med, Atlanta, GA 30322 USA

[2] Emory Univ, Grad Program Nutr Hlth Sci, Atlanta, GA 30322 USA

[3] Vanderbilt Univ, Med Ctr, Vanderbilt Eye Inst, Nashville, TN 37232 USA

[4] Emory Univ, Transgen Mouse Facil, Atlanta, GA 30322 USA

[5] Emory Univ, Dept Pediat, Div Pulm Allergy Cyst Fibrosis & Sleep, Atlanta, GA 30322 USA

来源：

TOXICOLOGICAL SCIENCES | 2008年 / 105卷 / 01期

关键词：

transgenic mice; cell death mechanisms; apoptosis; necrosis; calcium;

D O I：

10.1093/toxsci/kfn116

中图分类号：

R99 [毒物学（毒理学）];

学科分类号：

100405 ;

摘要：

Thioredoxin-2 (Trx2) is a multifunctional, mitochondria-specific protein, which inhibits cell death. The mitochondrial permeability transition (MPT) is a distinct mechanism for cell death activated by oxidants and linked to both necrotic and apoptotic morphologies. We studied mitochondria from Trx2 transgenic mice to determine whether Trx2 protects against oxidant-induced MPT. All experiments were performed in isolated mitochondria. Results showed that Trx2 protected against MPT induced by exogenously added peroxide. Unexpectedly, Trx2 also protected against the MPT induced by Ca(2+) in the absence of added peroxide. The results indicate that in addition to protecting against oxidative stress, Trx2 is an endogenous regulator of the MPT.

引用

页码：44 / 50

页数：7

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