Elucidation of the mechanisms by which neurogenesis is impaired in dyslipidemic patients
Project/Area Number |
26350921
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Applied health science
|
Research Institution | National Defense Medical College |
Principal Investigator |
Ishizuka Toshiaki 防衛医科大学校(医学教育部医学科進学課程及び専門課程、動物実験施設、共同利用研究, 医学教育部医学科専門課程, 教授 (30399117)
|
Co-Investigator(Kenkyū-buntansha) |
鈴木 豪 防衛医科大学校(医学教育部医学科進学課程及び専門課程、動物実験施設、共同利用研究, 薬理学, 講師 (50649035)
渡辺 康裕 防衛医科大学校(医学教育部医学科進学課程及び専門課程、動物実験施設、共同利用研究, 薬理学, 名誉教授 (90127324)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 神経前駆細胞 / 神経分化 / 酸化LDL / LOX-1 / PKC / Aktリン酸化 / CREBリン酸化 / Aktリン酸化 / 神経幹細胞 / 酸化LDL受容体 |
Outline of Final Research Achievements |
We revealed that stimulation with oxidized LDL (ox-LDL) significantly suppressed the differentiation of mouse neural progenitor cells into neural cells. In addition, it was found that the effects of ox-LDL is due to the activation of LOX-1 which activates PKC and inhibits the phosphorylation of Akt and CREB. Thus, the modulation of LOX-1 may ameliorate the impaired neurogenesis and neuropsychiatric function in dyslipidemic patients.
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Report
(4 results)
Research Products
(25 results)