| Project/Area Number |
15K14966
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pharmacology in pharmacy
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| Research Institution | Nihon University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
須川 晃資 日本大学, 理工学部, 准教授 (40580204)
小菅 康弘 日本大学, 薬学部, 准教授 (70383726)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | PGE2 / 運動ニューロン / グラフェン / 神経突起 / ALS / 細胞分化 / 突起進展 / ナノグラフェン / パッチクランプ法 / PGE2受容体 / ナノ粒子 / 細胞毒性 |
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| Outline of Final Research Achievements |
Prostaglandin E2 (PGE2) is a lipid mediator that plays important roles in various physiological and pathophysiological processes in the brain and spinal cord. We found that PGE2 promotes neurite outgrowth and suppresses cell proliferation by activating the PGE2 receptor EP2 subtype, and that the Gs protein-coupled cAMP-signaling pathway is involved in PGE2-induced differentiation of NSC-34 cells, a mouse motor neuron-like cell line. Moreover, we demonstrated the expression of EP2 in motor neurons is selectively increased in the lumbar spinal cord of ALS model mice at the symptomatic stage. Our in vitro approach using differentiated-NSC-34 cells has shown that PGE2 is involved in up-regulation of EP2 in these cells, and that PGE2-induced EP2 up-regulation in motor neurons may exacerbate the neuronal damage in ALS.
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