| Project/Area Number |
16K19375
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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 |
Gastroenterology
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| Research Institution | Kurume University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 炎症性腸疾患 / 胆汁酸 / 異所性発現 / 活性化誘導シチジンデアミナーゼ / AID / エピジェネティクス / AICDA / DNAメチル化 / クローン病 / メチル化 |
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| Outline of Final Research Achievements |
This study aims to elucidate whether gene expression, which changes by ectopically expressed AID (activation induced cytidine deaminase) in colonic epithelial cells (CECs), is induced by leaked bile acids under inflammatory conditions. Here we found that AID is ectopically expressed by treatment of bile acid in colon cancer cell lines. However, the mutually altered genes between AID stable expressing cell line and CECs from mice under inflammatory conditions could not be identified. Therefore, we next focused on gene expression profiles comparing wild type mice and AID deficient mice. Interestingly, we revealed that loss of AID in CECs from mice under inflammatory conditions is associated with altered gene expression, including the extracellular matrix-associated molecules.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、腸管の上皮細胞で異所性に発現するAIDが、細胞の生存環境に重要な足場を構成する遺伝子の発現に寄与していることを同定した。この足場は、細胞の増殖や維持、そして組織修復と多岐にわたり重要な役割を担っていることが知られている。つまり、炎症に伴い発現するAIDの役割を理解することは、おなかを健康に保つために重要であり、新たな治療法の確立にも貢献することが期待できると考えられる。
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