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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, 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
- Molecules and Cells, 36(3), 258-266
- Article Type
- Animal; Animal Cell; Animals; Apoptosis; Apoptosis-Inducing Factor; Brain Mitochondrion; C57Bl Mouse; Cell Viability; Controlled Study; Cytochrome C; Cytochromes C; Cytotoxicity; Encephale Isole; Hela Cell; Hela Cell Line; Hela Cells; Human; Human Cell; Humans; In Vitro Study; Male; Membrane Potential, Mitochondrial; Metabolism; Mice, Inbred C57BL; Mitochondria; Mitochondrial Membrane; Mitochondrial Membrane Potential; Mitochondrial Membranes; Mitochondrial Permeability Transition Pore; Mitochondrion; Mouse; Nerve Cell; Nerve Cell Membrane Steady Potential; Nerve Cell Necrosis; Neuronal Cell Death; Neurons; Nicotinamide Adenine Dinucleotide Adenosine Diphosphate Ribosyltransferase; Non-Human; Parp1 Protein, Human; Physiology; Poly(Adenosine Diphosphate Ribose); Poly(ADP-Ribose) Polymer; Poly(ADP-Ribose) Polymerase-1, Mouse; Poly(ADP-Ribose) Polymerase 1, Mouse; Poly(ADP-Ribose) Polymerases; Polymer; Polymers; Unclassified 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
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- Brain and Cognitive SciencesLaboratory of Neuronal Cell Death1. Journal Articles
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