Study for chromatin dynamics during optic nerve regeneration
| Project/Area Number |
25462753
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Ophthalmology
|
|---|
| Research Institution | Suzuka University of Medical Science (2014-2015)
Kanazawa University (2013) |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
|---|
| Keywords | 神経再生 / エピジェネティクス / レチノイン酸受容体 / ヒストンアセチル化 / 視神経 / 網膜神経節細胞 / 神経回路 / 中枢神経 / 中枢神経再生 / クロマチンリモデリング / 緑内障 / 生存 / 神経節細胞 |
|---|
| Outline of Final Research Achievements |
Like other CNS neurons, mature retinal ganglion cells (RGCs) cannot regenerate their axons after nerve injury due to loss of regenerative capacity. One of the reasons why they lose their capacity seems to be a dramatic shift in gene expression of RGCs under epigenetic modulation. In here, we found that levels of histone H3 lysine 9 acetylation decreased after birth in RGCs. This decrease showed good correlation with restriction of retinoic acid receptor β (RARβ) expression in RGCs after birth. Furthermore, we demonstrated that a histone deacetylase inhibitor, trichostatin A, induced axonal regeneration of adult rat RGCs through RARβ induction.
|
Report
(4 results)
Research Products
(24 results)
