| Project/Area Number |
16K20324
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Ophthalmology
|
|---|
| Research Institution | Kyoto Prefectural University of Medicine |
|---|
Principal Investigator |
Kitazawa Koji 京都府立医科大学, 医学(系)研究科(研究院), 特任助教 (10760803)
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | OVOL2 / PAX6 / 角膜上皮 / 転写因子 / リプログラミング / 分化 / 細胞運命 / KLF4 / コア転写因子 / ダイレクトリプログラミング |
|---|
| Outline of Final Research Achievements |
Functional analysis of core transcription factor in human corneal epithelial cells (CECs) revealed that CECs with OVOL2 knockdown became fibroblast-like cells, and OVOL2 knockdown reduced the expression of CEC-specific genes including keratin (K) 12 and E-cadherin, and the barrier function of CECs as measured by transepithelial electrical resistance. Next, when PAX6, which is an important transcription factor for eye development, was depleted by CRISPR/Cas9 targeted for PAX6 in human CECs, CEC-related gene including K12 and K3, was down-regulated, while K1 and K10, which were skin-related genes were up-regulated. These results suggest that PAX6 and OVOL2 were required for the terminal differentiation of CECs and, maintained the CEC identity.
|
