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Mol. Cells 2013; 36(3): 258-266

Published online September 30, 2013

https://doi.org/10.1007/s10059-013-0172-0

© The Korean Society for Molecular and Cellular Biology

Induction of Mitochondrial Dysfunction by Poly(ADP-Ribose) Polymer: Implication for Neuronal Cell Death

Seung-Hoon Baek, Ok-Nam Bae, Eun-Kyoung Kim, and Seong-Woon Yu

Department of Brain Science, Daegu Gyeongbuk Institute of Science and Technology (DGIST), Daegu 711-873, Korea, 1College of Pharmacy, Ajou University, Suwon 443-749, Korea, 2College of Pharmacy, Hanyang University, Ansan 426-791, Korea, 3These authors contributed equally to this work.

Received: June 5, 2013; Revised: June 22, 2013; Accepted: July 1, 2013

Abstract

Poly(ADP-ribose) polymerase-1 (PARP-1) mediates neu-ronal 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, sig-nals 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.

Keywords apoptosis-inducing factor, mitochondria, neuronal cell death, poly(ADP-ribose) polymer

Article

Research Article

Mol. Cells 2013; 36(3): 258-266

Published online September 30, 2013 https://doi.org/10.1007/s10059-013-0172-0

Copyright © The Korean Society for Molecular and Cellular Biology.

Induction of Mitochondrial Dysfunction by Poly(ADP-Ribose) Polymer: Implication for Neuronal Cell Death

Seung-Hoon Baek, Ok-Nam Bae, Eun-Kyoung Kim, and Seong-Woon Yu

Department of Brain Science, Daegu Gyeongbuk Institute of Science and Technology (DGIST), Daegu 711-873, Korea, 1College of Pharmacy, Ajou University, Suwon 443-749, Korea, 2College of Pharmacy, Hanyang University, Ansan 426-791, Korea, 3These authors contributed equally to this work.

Received: June 5, 2013; Revised: June 22, 2013; Accepted: July 1, 2013

Abstract

Poly(ADP-ribose) polymerase-1 (PARP-1) mediates neu-ronal 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, sig-nals 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.

Keywords: apoptosis-inducing factor, mitochondria, neuronal cell death, poly(ADP-ribose) polymer

Mol. Cells
Nov 30, 2022 Vol.45 No.11, pp. 763~867
COVER PICTURE
Naive (cyan) and axotomized (magenta) retinal ganglion cell axons in Xenopus tropicalis (Choi et al., pp. 846-854).

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