2020 Fiscal Year Final Research Report
Epigenetic regulation through estrogen and its receptors in inflammatory bowel disease model
| Project/Area Number |
19K16477
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 48010:Anatomy-related
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| Research Institution | University of Miyazaki |
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Principal Investigator |
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| Project Period (FY) |
2019-04-01 – 2021-03-31
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| Keywords | estrogen / epigenetics / colitis |
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| Outline of Final Research Achievements |
The results of this study suggest that estrogen has protective effect in colitis through its receptor ERβ and GPR30. Estrogen signaling acts through both genomic and non-genomic pathways. Moreover, epigenetic regulator HDAC, suberoylanilide hydroxamic acid attenuates inflammatory changes in DSS-induced colitis by suppressing local secretion of pro-inflammatory cytokines and chemokines and also by suppressing mobilization and accumulation of inflammatory cells. Detailed epigenetic analysis was detected that H3K36 expression was associated with colonic inflammation.
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| Free Research Field |
解剖学
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| Academic Significance and Societal Importance of the Research Achievements |
Estrogen targeted epigenetic therapy will help to develop new treatment approach for inflammatory bowel disease. Our results clearly indicated that estrogen has protective effect through its receptor GPR30 in mouse colitis model.
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