2017 Fiscal Year Final Research Report
Cyclosporine protects from apoptosis-mediated epithelial damage through epithelial STAT3 signaling pathway
| Project/Area Number |
26460957
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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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| Research Field |
Gastroenterology
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| Research Institution | Hirosaki University |
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Principal Investigator |
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| Research Collaborator |
HIRAGA Hiroto 弘前大学, 大学院医学研究科, 助教 (80637546)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Keywords | 炎症性腸疾患 / IL-22受容体 / TGF-beta / シクロスポリン / 腸上皮細胞 / アポトーシス |
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| Outline of Final Research Achievements |
Treatment of cyclosporine ameliorated mucosal destruction through reduction of epithelial apoptosis in DSS-induced colitis model. IL-22 receptor expression and STAT3 phosphorylation in purified intestinal epithelial cells (IECs) were up-regulated in cyclosporine but not in vehicle treated mice. Anti-TGF-beta mAb treatment diminished the protective effect of cyclosporine. In addition, anti-TGF-beta mAb treatment diminished up-regulated IL-22 receptor expression and STAT3 phosphorylation in IECs. In Caco2 cells, the treatment with both cyclosporine and recombinant TGF-beta increased IL-22 receptor expression. These results demonstrate that treatment of cyclosporine can ameliorate apoptosis-mediated epithelial damage through epithelial IL-22 receptor-STAT3 signaling pathway, which required the TGF-beta stimulation.
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| Free Research Field |
炎症性腸疾患
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