| Project/Area Number |
25461331
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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 |
Metabolomics
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| Research Institution | Chiba University |
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Principal Investigator |
KURODA Masayuki 千葉大学, 医学部附属病院, 特任准教授 (00253005)
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| Co-Investigator(Kenkyū-buntansha) |
KUBOTA Yoshitaka 千葉大学, 医学部附属病院, 講師 (10375735)
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| Co-Investigator(Renkei-kenkyūsha) |
BUJO Hideaki 東邦大学, 医療センター佐倉病院, 教授 (80291300)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 脂肪幹細胞 / 脂肪組織 / アルツハイマー認知症 / ネプリライシン / アルツハイマー / 脂肪細胞 / アミロイドβ / アルツハイマー病 / BDNF |
|---|
| Outline of Final Research Achievements |
To elucidate self-defensive mechanisms against amyloid β protein (Aβ) in adipose-tissue, cellular responses of adipose-derived stem cells (ASC) and progenitor cells (ccdPA) to Aβ were examined. Proliferation of ASC was enhanced and migration-related gene expression in ASC was increased upon low dose Aβ exposure. The gene expression was increased by NEP gene knock-down in ASC, but not in ccdPA, and decreased by NEP overexpression in ASC. NEP knock-down resulted in reduced lipid-droplet accumulation upon adipogenic stimulation in both cells.
These data indicated that ASC and ccdPA respond differently to Aβ, and suggested that adipose tissue regulates self-defensive mechanisms against Aβ through NEP-mediated signaling.
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