| Project/Area Number |
25293241
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SHIMADA Hiroki 金沢医科大学, 医学部, 講師 (60278108)
SHOJI Hiroki 金沢医科大学, 一般教育機構, 准教授 (10263873)
島村 英理子 金沢医科大学, 医学部, 講師 (00267741)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2015: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2013: ¥10,270,000 (Direct Cost: ¥7,900,000、Indirect Cost: ¥2,370,000)
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| Keywords | 母体免疫 / 白血病抑制因子 / インターロイキン６ / ＤＯＨａＤ / 自閉症スペクトラム / 副腎皮質刺激ホルモン / 胎盤 / DOHaD |
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| Outline of Final Research Achievements |
We previously described that the maternal-fetal leukemia inhibitory factor (LIF) signal relay contributes to the brain development of embryos in mice and rats. In the present study, we investigated the effects of maternal inflammation on the maternal-fetal LIF signal relay. To assess the effects of maternal inflammation, immunologically activated model mice were used. Pregnant mice were administered with polyinosinic:polycytidylic acid(Poly I:C). The administration of Poly I:C mimics influenza virus infections. The downstream signaling of LIFR/gp130 was inhibited by SOCS3, which was induced by excess inflammatory signals in the placenta. Thus, the signal tuning system of SOCS3 seems to protect fetuses from maternal inflammatory signals. However, the SOCS3 system also inhibited the physiological fetal-maternal signal relay; as a result, the development of the fetal cerebral cortex was damaged because of the starvation of LIF signals.
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