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Induction of mitochondrial dysfunction by poly(ADP-ribose) polymer: implication for neuronal cell death.
Seung-Hoon Baek1, Ok-Nam Bae, Eun-Kyoung Kim
1College of Pharmacy, Ajou University, Suwon, 443-749, Korea.
Molecules and Cells
|September 3, 2013
Summary
Poly(ADP-ribose) polymerase-1 (PARP-1) produces poly(ADP-ribose) (PAR) polymer, an endogenous mitochondrial toxin. PAR polymer triggers AIF release and neuronal cell death by damaging mitochondria.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Poly(ADP-ribose) polymerase-1 (PARP-1) activation is implicated in neuronal cell death following DNA damage.
- Poly(ADP-ribose) (PAR) polymer, a product of PARP-1, is hypothesized to mediate this cell death, potentially through mitochondrial pathways.
Purpose of the Study:
- To elucidate the specific effects of PAR polymer on mitochondria in neuronal cells.
- To investigate the role of PAR polymer in mitochondrial dysfunction and AIF release.
Main Methods:
- Experiments were conducted using cells in situ and isolated brain mitochondria in vitro.
- Mitochondrial membrane potential and mitochondrial permeability transition pore opening were assessed.
- The release of apoptosis-inducing factor (AIF) and cytochrome c from isolated mitochondria was analyzed.
Main Results:
- PAR polymer treatment led to early depolarization of mitochondrial membrane potential.
- PAR polymer induced the opening of the mitochondrial permeability transition pore.
- Specifically, PAR polymer triggered the release of AIF, but not cytochrome c, from isolated brain mitochondria.
Conclusions:
- PAR polymer acts as an endogenous mitochondrial toxin.
- These findings enhance the understanding of the PARP-1-dependent neuronal cell death pathway involving mitochondrial damage.
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