| Project/Area Number |
15591740
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Saitama Medical School (2005)
Nagoya University (2003-2004) |
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Principal Investigator |
ITAKURA Atsuo Saitama Medical School, Professor, 医学部, 教授 (70262897)
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| Co-Investigator(Kenkyū-buntansha) |
OKADA Mayumi Nagoya University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (90324433)
水谷 栄彦 名古屋大学, 大学院・医学系研究科, 教授 (00159162)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | angitensin II / trophoblast / extravillous trophoblast / choriocarcinoma / pregnancy induced hypertension / cytotrophoblast / 妊娠中毒症 |
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| Research Abstract |
Angiotensin II (Ang II), a bioactive peptide active in the renin-angiotensin system (RAS), has various biological functions besides its role as a potent vasoconstrictor. It has been shown to inhibit human extravillous trophoblast migration via PAI-1 activation through the Ang II type 1 receptor (AT1R). But, our previous study revealed induction of choriocarcinoma cell proliferation. The data suggested an involvement of the local RAS in tumor growth, contrasting with suppression of extravillous trophoblast invasion by RAS activation. In the present study we therefore investigated the effects of Ang II on choriocarcinoma cell migration in vitro using Boyden chamber and invasion assays. Ang II (10^<-8>M) promoted migration and invasion by a choriocarcinoma cell line (BeWo) and augmented random cell mobility on checker board analysis. Immunoblotting showed that Ang II activated the phosphorylation of FAK,ERK 1/2, and Akt in BeWo cells. Furthermore the Ang II effects on cell migration and invasion were abolished by a selective AT1R antagonist and an Akt inhibitor. The present results suggest that Ang II induced migration and invasion of choriocarcinoma cell probably involves PI3K/Akt following binding to the AT1R.
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