Regulation of tissue morphogenesis and pathology by miR-199a/214

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460357
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General medical chemistry
• Research Institution: The University of Tokyo
• Principal Investigator: Uchijima Yasunobu 東京大学, 大学院医学系研究科(医学部), 助手 (90272426)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: micro RNA / miR-199a / miR-214 / 形態形成 / 心筋線維化

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.

Free Research Field

分子形態形成