| Project/Area Number |
25861003
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Psychiatric science
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| Research Institution | Osaka University |
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Principal Investigator |
UMEDA-YANO Satomi 大阪大学, 医学(系)研究科(研究院), 特任研究員 (00625329)
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| Research Collaborator |
HASHIMOTO Ryota 大阪大学, 大学院連合小児発達学研究科, 准教授 (10370983)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | miR-137 / 統合失調症 / 神経細胞 / 分化 / 突起進展 / マウス初代神経細胞 / 中間表現型 / 遺伝子 / SH-SY5Y細胞 / レチノイン酸 / BDNF |
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| Outline of Final Research Achievements |
A recently completed genome-wide association study (GWAS) showed that single-nucleotide polymorphisms (SNPs) in the MIR137 gene, which encodes one of the brain-enriched miRNAs (miR-137), is highly associated with schizophrenia. In addition, the GWAS showed that not only miR-137 but also putative target genes of miR-137 (CSMD1, C10orf26, CACNA1C and TCF4) have significant associations with schizophrenia. Further, genes which have been reported to be associated with schizophrenia are enriched in predicted miR-137 target genes. In this study, we investigated the role of miR-137 and its target genes during neuronal differentiation. Our results showed that miR-137 expression increased during neuronal differentiation, but miR-137 does not seem to be involved in it. Further, miR-137 does not regulate the expression of CSMD1, C10orf26, CACNA1C and TCF4 in neuroblastoma cells and primary neurons.
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