| Project/Area Number |
23580134
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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 |
Applied biochemistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
YANAKA NORIYUKI 広島大学, 生物圏科学研究科, 准教授 (70346526)
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| Co-Investigator(Kenkyū-buntansha) |
NORIHISA Kato 広島大学, 大学院生物圏科学研究科, 教授 (20144892)
MASANOBU Wada 広島大学, 大学院総合科学研究科, 教授 (80220961)
TOMOHIRO Kurisaki 京都大学, 再生医科学研究所, 助教 (90311422)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 脂肪細胞 / コリン / グリセロホスホコリン / 浸透圧 / 増殖 / choline / glycerophosphocholine / 3T3-L1 / clonal expansion / C2C12細胞 / 骨格筋細胞 / 筋分化 |
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| Research Abstract |
We previously showed that GDE5 is a cytosolic glycerophosphocholine (GPC) phosphodiesterase. Here, we characterized the cellular functions of GDE5 in adipocytes because GDE5 expression is highly expressed during 3T3-L1 adipocyte differentiation. Knockdown of endogenous GDE5 in 3T3-L1 adipocytes dramatically suppressed adipocye differentiation, unexpectedly, through a modulation of the mitotic clonal expansion. Decreasing GDE5 abundance resulted in a marked increase in intracellular GPC level. We showed that decreasing GDE5 expression significantly upregulated mRNA expression of proteoglycans such as lumican, and decorin in 3T3-L1 cells. These results suggest that decreasing GDE5 abundance caused osmotic imbalance by the intracellular GPC accumulation and inhibited the mitotic clonal expansion of adipocytes. These provide an insight into the novel roles of GDE5 in osmotic balance which depends on GPC phosphodiesterase activity.
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