| Project/Area Number |
20591931
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Obstetrics and gynecology
|
|---|
| Research Institution | Nippon Medical School |
|---|
Principal Investigator |
TAKESHITA Toshiyuki (2009-2010) Nippon Medical School, 大学院・医学研究科, 教授 (60188175)
羅 善順 (2008) Nippon Medical School, 医学部, 助教 (60339439)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
ISHIBASHI Osamu 日本医科大学, 医学部, 講師 (70293214)
KIKUCHI Kunio 日本医科大学, 医学部, 助教 (70374676)
TOMIYAMA Ryoko 日本医科大学, 医学部, 医療技術員 (40409214)
竹下 俊行 日本医科大学, 大学院・医学研究科, 教授 (60188175)
森 美貴 日本医科大学, 医学部, 助教 (00277576)
原田 明希摩 日本医科大学, 医学部, 研究技術員 (70535426)
|
|---|
| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 卵巣 / 卵胞顆粒膜細胞 / マイクロRNA / 生殖医学 / microRNA |
|---|
| Research Abstract |
We performed large-scale profiling of microRNA (miRNAs) in human granulosa-derived cell lines (e.g., KGN) by high-throughput sequencing. In these cell lines, we found that miR-21 accounted for more than 80% of AGO2 (designated EIFC2) -bound miRNAs, suggesting that it played a central role as a functional miRNA in human GCs. We also performed cDNA cloning of AGO2-bound mRNAs in KGN cells and identified COL4A1 mRNA as a possible miR-21 target in KGN cells, which was corroborated by subsequent experimental validation. In proceeding in vitro functional studies using synthetic mimics of miRNA precursors or short-interference RNAs, we also found that these short double-strand RNAs (23- and/or 24-nucleotide dsRNAs) readily induced apoptosis in human granulosa cell tumor-derived cells but not in other cell types. Furthermore, we revealed that the short dsRNAs transcriptionally hyper-induce retinoic acid-inducible gene-I through dsRNA-activated protein kinase.
|
