2011 Fiscal Year Final Research Report
Neuronal cell death mediated by mitochondria
| Project/Area Number |
21659018
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | Kanazawa University |
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Principal Investigator |
YONEDA Yukio 金沢大学, 薬学系, 教授 (50094454)
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| Project Period (FY) |
2009 – 2011
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| Keywords | ミトコンドリア / 神経細胞死 / NMDA / グルタミン酸 / 脳虚血 |
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| Research Abstract |
Glutamate neurotoxicity was found to at least in part involve mitochondrial membrane potential disruption, mPTP orchestration, mitochondrial free Ca^<2+> levels and UCP2 expression in rat hippocampal and cortical neurons. In HEK293 cells with acquired NMDAR channels and overexpressed UCP2, a more marked increase was seen in mitochondrial free Ca^<2+> levels, in addition to more severe cell death, after the exposure to NMDA than in cells without UCP2 overexpression. Accordingly, UCP2 could play a role as a determinant of the neurotoxicity mediated by NMDAR through a mechanism related to the modulation of mitochondrial free Ca^<2+> levels in neurons.
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[Journal Article] Positive regulation of osteoclastic differentiation by growth differentiation factor-15 up-regulated in osteocytic cells under hypoxia2012
Author(s)
Hinoi E, Ochi H, Takarada T, Nakatani E, Iezaki T, Nakajima H, Fujita H, Takahata Y, Hidano S, Kobayashi T, Takeda S & Yoneda Y
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Journal Title
J Bone Miner Res
Volume: (in press)
DOI
Peer Reviewed
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