Potential mechanism by which glucose regulates decidualization
| Project/Area Number |
15K20145
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Obstetrics and gynecology
|
|---|
| Research Institution | Yamaguchi University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2015-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 脱落膜化 / グルコース / ヒストン修飾 / 転写因子 / エピジェネティクス / 子宮内膜 / インスリンシグナル |
|---|
| Outline of Final Research Achievements |
The present study showed the detailed mechanisms that glucose regulates the expression of FOXO1 through the increase of H3K27ac undergoing decidualization in human ESCs. In addition, glucose also regulates H3K27ac of the PRL and IGFBP-1 promoter regions during decidualization, which is crucial for the acceptance of transcriptional factors to the promoter regions.
Decidualization stimuli activate the insulin signaling-regulated genes, which contribute to proper decidualization through the increase of glucose uptake.
|
Report
(3 results)
Research Products
(7 results)
