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

Induction of mitochondrial dysfunction by poly(ADP-ribose) polymer: Implication for neuronal cell death
Baek, Seung-HoonBae, Ok-NamKim, Eun-KyoungYu, Seong-Woon
DGIST Authors
Kim, Eun-KyoungYu, Seong-Woon
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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
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.
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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