Modeling the neural impact of maternal immune modulation using human induced pluripotent stem cells.
Project/Area Number |
15K09719
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Embryonic/Neonatal medicine
|
Research Institution | Kyoto Prefectural University of Medicine |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
千代延 友裕 京都府立医科大学, 医学(系)研究科(研究院), 助教 (40571659)
|
Research Collaborator |
ZUIKI Masashi
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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Keywords | iPS 細胞 / インターロイキン6 / 神経分化 / 神経凝集体 / ルテオリン |
Outline of Final Research Achievements |
We induced differentiation of iPS cells derived from healthy individuals into neuroectodermal cells. We then cultured these iPS cells in suspension cultures to obtain neuronal aggregates. Based on the shift of neuronal cell markers, we confirmed that these neuronal aggregates were emulating the cerebral cortex. When we exposed this fetal brain model to interleukin-6 (IL-6) for 24 hours, we observed increased levels of phosphorylated signal transducer and activator of transcription 3 (STAT3). Ten days later, we found increased levels of astrocytes and a reduction in neuronal cells. Simultaneous administration of luteolin downregulated the phosphorylation of STAT3 and inhibited the attenuation in neuronal differentiation induced by IL-6. We believe the neuronal system model used in this study can greatly contribute to the pathophysiological analysis and treatment discovery in fetal encephalopathy caused by the fetal environment.
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Report
(4 results)
Research Products
(3 results)