| Project/Area Number |
18591794
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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 | Gunma University |
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Principal Investigator |
ABE Yumiko Gunma University, School of Medicine, Associate Professor (70261857)
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| Co-Investigator(Kenkyū-buntansha) |
MINEGISHI Takashi Gunma University, Graduate School of Medicine, Professor (00209842)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥1,950,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥150,000)
Fiscal Year 2007: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2006: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | chorioamnionitis / inhibin / activin / dioxin / comprehensive analysis / microarray / quantitative PCR / real-time PCR |
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| Research Abstract |
Activins are dimeric proteins composed of inhibin/activin beta-subunits, and their biological activities are regulated by inhibins, and activinbinding proteins called follistatins. Recently, the involvement of activins in inflammation and wound healing has been reported. In order to study the role of inhibin/activin family proteins in chorioamnionitis, which is the primary cause of premature rupture of the membranes, we used human amniotic cell culture with the permission of The Internal Review Board and the informed consent of the patients. We studied gene expressions in amniotic epithelial cells by DNA microarray and quantitative PCR analyses, and detected interferon-inducible genes and genes related to collagen synthesis or degradation as dioxin-inducible genes. DNA microarray analysis showed increased expression of the inhibin/activin beta A subunit also. The involvement of activins in the pathology of membranes by dioxins was suggested. In order to study if activins were involved in the inflammation in the compact layer and the fibroblast layer of the membranes, amniotic mesenchymal cells were studied. Tumor necrosis factor-alpha (TNF-alpha) did not increase the inhibin/activin beta B subunit mRNA but did increase the inhibin/activin beta A subunit mRNA. The increase of activin A protein was also shown by enzyme linked immunosorbent assay. Inflammatory cytokine TNF-alpha seemed to stimulate the production of activin A at both mRNA and protein levels in these cells.
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