| Project/Area Number |
24659146
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MATSUURA Ken 東京大学, 分子細胞生物学研究所, 助教 (10625742)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 細胞融合 / 胎盤 / 組織修復 / 組織再生 / 浸潤 / 転移 / Wnt / Bcl9-like / Gcm1 / Syncytin / 組織修復・再生 / 浸潤・転移 |
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| Research Abstract |
We analyzed expression of GCM1, SynA and SynB, genes that are known to regulate cell fusion during placentation, in mouse tissues. We found that GCM1 and SynA are expressed several tissues besides placenta, including the brain, lung, liver, intestine, skin and kidney. This finding suggests that GCM1 and SynA are also involved in cell fusion in these tissues. We next examined whether GCM1, SynA and SynB are involved in cell fusion during repair and regeneration of injured tissues. We found that expression of GCM1, SynA and SynB are markedly up-regulated in the kidney injured by ischemia-reperfusion. Expression of SynA is also increased in the crypt of the intestine injured by ulcerative colitis. These results suggest that GCM1, SynA and SynB induce cell fusion during repair and regeneration of injured tissues. Our findings may contributes to protection of the transplanted organ from ischemia-reperfusion injury.
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