2022 Fiscal Year Final Research Report
Novel function "regulation of extracellular matrix construction" of ectopic AID expression in wound healing process.
| Project/Area Number |
20K08318
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 53010:Gastroenterology-related
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| Research Institution | Kurume University |
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Principal Investigator |
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| Project Period (FY) |
2020-04-01 – 2023-03-31
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| Keywords | 炎症性腸疾患 / AID / 異所性発現 |
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| Outline of Final Research Achievements |
To evaluate the role of AID, which is ectopically expressed in colonic epithelial cells (CECs) under inflammatory conditions, wild-type (WT) and AID-deficient mice were evaluated using the DSS-induced colitis model. Restoration of body weight loss after colitis induction is delayed in AID-deficient mice compared to WT mice. In addition, the expression of extracellular matrix-associated molecules in CECs of WT and AID-deficient mice transitioned to the recovery phase was not only significantly altered, but also the disease score of colon tissue was significantly higher in AID-deficient mice compared to WT mice. Additionally, we found that AID, which is ectopically expressed under inflammation conditions, binds to target genes and induces DNA demethylation, possibly regulating the expression of those genes using colorectal cancer cell lines stably expressing AID.
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| Free Research Field |
粘膜免疫
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| Academic Significance and Societal Importance of the Research Achievements |
本研究成果より、炎症に伴って大腸上皮細胞に異所性発現するAIDの役割を理解することは、大腸粘膜を治癒(創傷治癒過程)させるためのメカニズムを理解するための一助になることが期待できると考えられる。さらに先行研究では異所性なAIDの発現は、上皮細胞の悪性転換に関与する可能性が報告がされていることからも、慢性炎症による発がん機構の解明にも貢献できる可能性が期待される。
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