The study of the repair mechanism by neuron and glial cell after central nervous system injury
Project/Area Number |
24592729
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Emergency medicine
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Research Institution | Fukushima Medical University (2013-2014) Yamagata University (2012) |
Principal Investigator |
ISEKI Ken 福島県立医科大学, 医学部, 教授 (70332921)
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Co-Investigator(Kenkyū-buntansha) |
GOTO Kaoru 山形大学, 医学部, 教授 (30234975)
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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 |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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Keywords | グリオーシス / 凍結脳損傷 / プロテオグリカン / 脂質代謝酵素 / 肝障害 / 核内脂質代謝酵素 / コンドロイチン硫酸プロテオグリカン / ヘパラン硫酸プロテオグリカン / 中枢神経 / アストロサイト / 脳損傷 / ニューロン / グリア |
Outline of Final Research Achievements |
Transcription factor OASIS controls the production of proteoglycan in embryonic development, whereas Olig is a key factor of glial differentiation. However, detailed repair mechanism after brain injury remains unclear. We investigated the expression pattern of these transcription factors after brain injury. Results suggest that OASIS is involved in the regulatory mechanism of non-permissive environments for axonal outgrowth and that Olig genes regulate glial differentiation. The expression pattern of the relevant molecules remained unchanged in KO mice of diacylglycerol kinase, an enzyme responsible for the control of a lipid messenger diacylglycerol.
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Report
(4 results)
Research Products
(9 results)
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[Journal Article] NMDA receptor-mediated Ca(2+) influx triggers nucleocytoplasmic translocation of diacylglycerol kinase ζ under oxygen-glucose deprivation conditions, an in vitro model of ischemia, in rat hippocampal slices2012
Author(s)
Suzuki Y, Yamazaki Y, Hozumi Y, Okada M, Tanaka T, Iseki K, Ohta N, Aoyagi M, Fujii S, Goto K.
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Journal Title
Histochem CellBiol
Volume: 137
Issue: 4
Pages: 499-511
DOI
Related Report
Peer Reviewed
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