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Induction of mitochondrial dysfunction by poly(ADP-ribose) polymer: Implication for neuronal cell death

Title
Induction of mitochondrial dysfunction by poly(ADP-ribose) polymer: Implication for neuronal cell death
Author(s)
Baek, Seung-HoonBae, Ok-NamKim, Eun-KyoungYu, Seong-Woon
Issued Date
2013-09
Citation
Molecules and Cells, v.36, no.3, pp.258 - 266
Type
Article
Author Keywords
Apoptosis-inducing factorMitochondriaNeuronal cell deathPoly(ADP-ribose) polymer
Keywords
APOPTOSIS-INDUCING FACTORPERMEABILITY TRANSITION POREPAR POLYMERCLEAVAGE
ISSN
1016-8478
Abstract
Poly(ADP-ribose) polymerase-1 (PARP-1) mediates neuronal cell death in a variety of pathological conditions involving severe DNA damage. Poly(ADP-ribose) (PAR) polymer is a product synthesized by PARP-1. Previous studies suggest that PAR polymer heralds mitochondrial apoptosis-inducing factor (AIF) release and thereby, signals neuronal cell death. However, the details of the effects of PAR polymer on mitochondria remain to be elucidated. Here we report the effects of PAR polymer on mitochondria in cells in situ and isolated brain mitochondria in vitro. We found that PAR polymer causes depolarization of mitochondrial membrane potential and opening of the mitochondrial permeability transition pore early after injury. Furthermore, PAR polymer specifically induces AIF release, but not cytochrome c from isolated brain mitochondria. These data suggest PAR polymer as an endogenous mitochondrial toxin and will further our understanding of the PARP-1-dependent neuronal cell death paradigm. © The Korean Society for Molecular and Cellular Biology. All rights reserved.
URI
http://hdl.handle.net/20.500.11750/3212
DOI
10.1007/s10059-013-0172-0
Publisher
Korean Society for Molecular and Cellular Biology
Related Researcher
  • 김은경 Kim, Eun-Kyoung 뇌과학과
  • Research Interests Neural functions in metabolic diseases; 뇌신경세포와 비만; 당뇨 등의 대사 질환 관련 연구
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Appears in Collections:
Department of Brain Sciences Lab of Neuro-Metabolism & Neurometabolomic Research Center 1. Journal Articles
Department of Brain Sciences Laboratory of Neuronal Cell Death 1. Journal Articles

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