| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
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)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Outline of Final Research Achievements |
In Dnm3os Knock-out mice, Nrip1 mRNA was increased and this gene was considered as a candidate for the target of miR-214. In vitro analysis suggested Nrip1 may contribute to the phenotypes such as decreased size observed in the KO mice. Doxorubicin (Dox) induced myocardial injury and this was suppressed by knocking in miR-199a/214 into the Ednra locus. Because the participation of neural crest cell (NCC) was suggested for the rescue mechanism of myocardium injury, NCC derived embryonic heart cells were collected and subjected to the single cell transcriptome analysis. In these cells, some expressed several smooth muscle cell markers, and a few cells expressed progenitor cell markers such as Kit, Sox10, and Pax3. The latter cells were expected to contribute to the protection from myocardium injury.
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