Project/Area Number |
20591907
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Obstetrics and gynecology
|
Research Institution | The University of Tokyo |
Principal Investigator |
FUJII Tomoyuki The University of Tokyo, 医学部附属病院, 准教授 (40209010)
|
Co-Investigator(Kenkyū-buntansha) |
KAWANA Kei 東京大学, 医学部附属病院, 助教 (60311627)
兵藤 博信 東京大学, 医学部・附属病院, 助教 (00436495)
|
Co-Investigator(Renkei-kenkyūsha) |
HYODO Hironobu 東京大学, 医学部附属病院, 助教 (00436495)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 妊娠 / 胎盤 / 炎症 / CD1d / 不育症 / 抗リン脂質抗体 / invariant NKT / Interleukin-12 / 絨毛細胞 / オートタキシン |
Research Abstract |
To clarify the physsiological and pathological roles of inflammation system in placenta during pregnancy, we investigated the roles of CD1d antigen on trophoblasts and of lysophosphatidic acid (LPA) system in placenta. The decrease of CD1d expression on cytotrophoblasts with extravillous trophoblast (EVT) differentiation was induced via transforming growth factor (TGF)-・ secretion by trophoblasts. β_2-glycoprotein I (β_2GPI)-dependent anti-phospholipid antibody induced interleukin-12 release from trophoblasts via recognition of β_2GPI bound to phosphatidylserine on CD1d on trophoblasts, which might cause pregnancy loss via inflammatory mechanism. Trophoblasts expressed the major lysophosphatidic acid (PLA) producing enzyme, autotaxin (ATX). RNA amounts of ATX in placenta tissues increased with gestational weeks. The serum concentration of ATX protein was higher in patients with preterm labor than that in normal pregnant women. These results suggest the physiological roles of its bioactive resultant substance, LPA, during pregnancy.
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