2016 Fiscal Year Final Research Report
Potential mechanism by which glucose regulates decidualization
| Project/Area Number |
15K20145
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Yamaguchi University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Keywords | 脱落膜化 / グルコース / ヒストン修飾 / 転写因子 |
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| 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.
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| Free Research Field |
生殖内分泌
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