| Project/Area Number |
23592416
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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 |
Obstetrics and gynecology
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| Research Institution | Hamamatsu University School of Medicine (2012-2013)
Juntendo University (2011) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TANAK Toshitaka 順天堂大学, 医学部, 准教授 (30407283)
MAKINO Shintaro 順天堂大学, 医学部, 准教授 (70570894)
YORIFUJI Takasi 順天堂大学, 医学部, 助教 (10597058)
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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 |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 絨毛細胞 / ＣＤ４４ / シグナル伝達 / 再生 / CD44 / sFLT1 |
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| Research Abstract |
The function of CD44v3 and heparin/heparan sulphate (HS) signaling was investigated during trophoblast cell migration. We evaluated the effect of heparin/ HS/CD44v3-mediated processes during scratch wound closure in TCL-1 cells. An in vitro scratch wound healing assay showed enhanced migration of trophoblast cells in a dose-dependent manner in the presence of heparin compared with controls. Conversely, an anti-CD44 function blocking antibody and CD44siRNA suppressed the migration of trophoblast cells in the presence of heparin in a similar scratch assay. Both heparin treatment and in vitro scratch wounding induced the phosphorylation of p21-activated kinase 1 (PAK1), while the anti-CD44v3 antibody suppressed the heparin-induced phosphorylation of PAK1. These results indicate that heparin/heparan sulphate/CD44v3-mediated signaling, in the absence of growth factor networks, enhances the direct repair of the damaged trophoblast layer through the migration of trophoblast cells.
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