The functional analysis of novel non-coding RNAs in the differentiation of myogenic cells
Project/Area Number |
25860151
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
General anatomy (including histology/embryology)
|
Research Institution | Fujita Health University |
Principal Investigator |
Hitachi Keisuke 藤田保健衛生大学, 総合医科学研究所, 助教 (10508469)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | ノンコーディングRNA / 細胞分化 / RNA結合タンパク質 / 筋萎縮 / 骨格筋萎縮 |
Outline of Final Research Achievements |
In this study, we identified two novel non-coding RNAs (miR-191 and Myog pancRNA) involved in the regulation of myogenic differentiation. We found that miR-191 is essential for the differentiation of myogenic cell line (C2C12 cells). In addition to the miRNA, we also revealed that Myog pancRNA, expressed from the promoter region of myogenin gene, regulates the differentiation of C2C12 cells via the interaction with Ddx17 and hnRNPK proteins. Interestingly, knockdown of Ddx17 inhibited the C2C12 myogenic differentiation. On the other hand, knockdown of hnRNPK promoted the differentiation of C2C12 cells. We also found that the expression of Myog pancRNA is largely increased in atrophic skeletal muscle induced by denervation. Taken together, our results indicate that non-coding RNAs are new regulator of the myogenic cell differentiation, and suggest that Myog pancRNA is a new therapeutic target to improve skeletal muscle atrophy caused by denervation.
|
Report
(5 results)
Research Products
(9 results)