Mitochondrial apoptosis is amplified through gap junctions

被引：34

作者：

Peixoto, Pablo M. ^{[1
]}

Ryu, Shin-Young ^{[1
]}

Pruzansky, Dawn Pietkiewicz ^{[1
]}

Kuriakose, Maria ^{[2
]}

Gilmore, Andrew ^{[3
]}

Kinnally, Kathleen W. ^{[1
]}

机构：

[1] NYU, Coll Dent, Dept Basic Sci, New York, NY 10010 USA

[2] Amrita Inst Med Sci, Kochi, Kerala, India

[3] Univ Manchester, Welcome Trust Ctr Cell Matrix Res, Manchester, Lancs, England

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 390卷 / 01期

基金：

美国国家卫生研究院;

关键词：

Mitochondrial apoptosis; Gap junctions; MAC; Cytochrome c; tBid; Bystander effect; INDUCED CELL-DEATH; CYTOCHROME-C; CANCER; CHANNELS; CONDUCTANCE; VECTOR; GENE; MAC;

D O I：

10.1016/j.bbrc.2009.09.054

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：

The death of one cell can precipitate the death of nearby cells in a process referred to as the bystander effect. We investigated whether mitochondrial apoptosis generated a bystander effect and, if so, by which pathway. Microinjection with cytochrome c mimicked function of the mitochondrial apoptosis-induced channel MAC and caused apoptosis of both target and nearby osteoblasts. This effect was suppressed by inhibiting gap junction intercellular communication. A bystander effect was also observed after exogenous expression of tBid, which facilitates MAC formation and cytochrome c release. Interestingly, in connexin-43 deficient osteoblasts, microinjection of cytochrome c induced apoptosis only in the target cell. These findings indicate that a death signal was generated downstream of MAC function and was transmitted through gap junctions to amplify apoptosis in neighboring cells. This concept may have implications in development of new therapeutic approaches. (C) 2009 Elsevier Inc. All rights reserved

引用

页码：38 / 43

页数：6

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