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Inhibition of Alzheimer’s amyloid-beta peptide-induced reduction of mitochondrial membrane potential and neurotoxicity by gelsolin

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/714

Title: Inhibition of Alzheimer’s amyloid-beta peptide-induced reduction of mitochondrial membrane potential and neurotoxicity by gelsolin
Authors: Hongjiang, Qiao Browse this author
Richard, C. Koya Browse this author
Nakagawa, Koji Browse this author
Tanaka, Hiroki Browse this author
Fujita, Hisakazu Browse this author
Takimoto, Masato Browse this author
Kuzumaki, Noboru Browse this author
Keywords: gelsolin
Alzheimer disease
amyloid-beta
rat pheochromocytoma
mitochondrial membrane potential
cytotoxicity
cytochrome c
Issue Date: Jun-2005
Publisher: Elsevier
Journal Title: Neurobiology of Aging
Volume: 26
Start Page: 849
End Page: 855
Publisher DOI: 10.1016/j.neurobiolaging.2004.08.003
PMID: 15718043
Abstract: Amyloid-beta (Abeta) peptides play a central role in the development of Alzheimer’s disease. They are known to induce mitochondrial dysfunction and caspase activation, resulting in apoptosis of neuronal cells. Here we show that human cytoplasmic gelsolin inhibits Abeta peptide-induced cell death of neuronally differentiated rat pheochromocytoma (PC-12) cells. We also show that the segment 5 but not 6 of human cytoplasmic gelsolin is the important region responsible for inhibition of Abeta-induced cytotoxicity. Mitochondrial dysfunction associated with cell death, membrane potential loss and the release of cytochrome c are all abrogated in the presence of human full-length or segment 5 cytoplasmic gelsolin. Furthermore, RNA interference to reduce expression of endogenous gelsolin in PC12 cells shows that rat gelsolin act as an inhibitor of Abeta cytotoxicity. These results demonstrate that cytoplasmic gelsolin plays a important role in inhibiting Abeta-induced cytotoxicity by inhibiting apoptotic mitochondrial changes. The segment 5 of human cytoplasmic gelsolin is sufficient for the function.
Relation: http://www.sciencedirect.com/science/journal/01974580
Type: article (author version)
URI: http://hdl.handle.net/2115/714
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 葛巻 暹

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