2015 Fiscal Year Final Research Report
Analysis of novel transcriptional mechanisms and identification of non-coding RNAs contributing renal fibrosis.
| Project/Area Number |
26860627
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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 |
Kidney internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MIMURA IMARI 東京大学, 医学部附属病院, 助教 (00727084)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Keywords | 腎線維化 / 非翻訳RNA |
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| Outline of Final Research Achievements |
The main researcher of this project administered Dznep, which is one of inhibitors of histone repressive mark H3K27me3, to chronic kidney disease model mice in order to identify novel epigenetic mechanisms and factors which contribute to the reduction of tubulointerstitial fibrosis. I used laser captured microdissection to cut out only tubular cells from in vivo mice cortexes. I performed genome-wide analysis of RNA using high throughput sequencers. As a result, I identified changes of genes or lincRNAs expressions which are associated with renal fibrosis. These results suggested that there is a possibility that epigenetic factors driven by Dznep lead to amelioration of tubulointerstitial fibrosis.
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| Free Research Field |
腎臓
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