Study of neurotoxicity of activated human glial cells
| Project/Area Number |
24591721
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Shimane University |
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Principal Investigator |
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| Research Collaborator |
MCGEER Patrick L. University of British Columbia, Department of Psychiatry, Professor Emeritus
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ヒトグリア細胞 / 炎症性活性化 / 神経毒性 / ヒストン脱アセチル化酵素阻害剤 / L型カルシウム拮抗剤 / 国際研究者交流 / カナダ |
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| Outline of Final Research Achievements |
Using primary culture of human glial a cells, we studied inflammatory activation processes of glial cells, which induce neurotoxicity, and identified the drugs that inhibited the glial neurotoxicity. The histone deacetylase inhibitor suberoylanilide hydroxamic acid significantly attenuated the neurotoxicity of astrocytes activated by IFN-γ. L-type calcium channel blockers significantly suppressed neurotoxic secretions from activated human astrocytes and microglia. These drugs reduced the STAT3 phosphorylation at the tyrosine-705 residue in the IFN-γ-activated astrocytes.
These findings suggest that neurotoxicity of human astrocytes is mediated by STAT3 phosphorylationboth and that both histone deacetylase inhibitors and L-type calcium channel blockers could be a useful treatment option for a broad spectrum of neurodegenerative diseases. Moreover, the tyrosine-705 residue in STAT3 could be a molecular target to develop new drugs for treatment of neurodegenerative disorders.
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Report
(4 results)
Research Products
(11 results)
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[Journal Article] Minocycline improves recognition memory and attenuates microglial activation in Gunn rat: A possible hyperbilirubinemia-induced animal model of schizophrenia2014
Author(s)
Liaury K, Miyaoka T, Tsumori T, Furuya M, Hashioka S, Wake R, Tsuchie K, Fukushima M, Limoa E, Tanra AJ, Horiguchi J
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Journal Title
Progress in Neuro-Psychopharmacology & Biological Psychiatry
Volume: 50
Pages: 184-190
DOI
Related Report
Peer Reviewed
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