| Project/Area Number |
25461568
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Kurume University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUISHI TOYOJIRO 久留米大学, 医学部, 教授 (60157237)
TANAKA EIICHIRO 久留米大学, 医学部, 教授 (80188284)
MURAI YOSHINAKA 久留米大学, 医学部, 准教授 (20352122)
OKABE YASUNORI 久留米大学, 医学部, 助教 (00446098)
KUNISADA TAKAHIRO 岐阜大学, 医学系研究科, 教授 (30205108)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | レット症候群 / Rett症候群 / MeCP2 / Mecp2 / rett症候群 |
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| Outline of Final Research Achievements |
Rett syndrome (RTT) is a neurodevelopmetal disorder associated with mutations in the methyl-CpG－binding protein 2 (MeCP2) gene. Mecp2-deficient ES/iPS cells provide a powerful research tool for disease mechanism studies of RTT. In this study, we found that RTT model (Mecp2-null) ESCs could differentiate into astroglia, oligodendrocyte, and microglia. These results suggest that MeCP2 is not essential for induction of glial cell differentiation. Quantitative RT-PCR analysis revealed that some of microglia marker and cytokine signal genes were lower in Mecp2-null mice than in wild-type mice. These results indicate that loss of MeCP2 leads, either directly or indirectly, to transcriptional dysregulation of these genes in the differentiating microglia. In addition, to confirm the effects of MeCP2 deficiency on microglia function, we investigated the cytokine response and the phagocytic activity of the microglia derived from the wild-type or Mecp2-null cultures.
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