Cited 13 time in webofscience Cited 13 time in scopus

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
Authors
Baek, SH[Baek, Seung-Hoon]Bae, ON[Bae, Ok-Nam]Kim, EK[Kim, Eun-Kyoung]Yu, SW[Yu, Seong-Woon]
DGIST Authors
Kim, EK[Kim, Eun-Kyoung]Yu, SW[Yu, Seong-Woon]
Issue Date
2013-09
Citation
Molecules and Cells, 36(3), 258-266
Type
Article
Article Type
Article
Keywords
AnimalAnimal CellAnimalsApoptosisApoptosis-Inducing FactorBrain MitochondrionC57Bl MouseCell ViabilityControlled StudyCytochrome CCytochromes CCytotoxicityEncephale IsoleHela CellHela Cell LineHela CellsHumanHuman CellHumansIn Vitro StudyMaleMembrane Potential, MitochondrialMetabolismMice, Inbred C57BLMitochondriaMitochondrial MembraneMitochondrial Membrane PotentialMitochondrial MembranesMitochondrial Permeability Transition PoreMitochondrionMouseNerve CellNerve Cell Membrane Steady PotentialNerve Cell NecrosisNeuronal Cell DeathNeuronsNicotinamide Adenine Dinucleotide Adenosine Diphosphate RibosyltransferaseNon-HumanParp1 Protein, HumanPhysiologyPoly(Adenosine Diphosphate Ribose)Poly(ADP-Ribose) PolymerPoly(ADP-Ribose) Polymerase-1, MousePoly(ADP-Ribose) Polymerase 1, MousePoly(ADP-Ribose) PolymerasesPolymerPolymersUnclassified Drug
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
Files:
There are no files associated with this item.
Collection:
Brain and Cognitive SciencesLaboratory of Neuronal Cell Death1. Journal Articles


qrcode mendeley

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE