2017 Fiscal Year Final Research Report
Investigation of the mechanism of fibrosis in IgG4-related disease
Project/Area Number |
15K10818
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Otorhinolaryngology
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Research Institution | Sapporo Medical University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
松宮 弘 札幌医科大学, 医学部, 研究員 (80517904)
角木 拓也 札幌医科大学, 医学部, 研究員 (70706548)
金子 躍人 札幌医科大学, 医学部, 研究員 (90738874)
矢島 諒人 札幌医科大学, 医学部, 研究員 (90722455)
垣内 晃人 札幌医科大学, 医学部, 研究員 (60722436)
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Project Period (FY) |
2015-04-01 – 2018-03-31
|
Keywords | 唾液腺 / IgG4関連疾患 / 線維化 / 繊維芽細胞 / IL-6 |
Outline of Final Research Achievements |
In GeneChip analysis, mRNAs of IL-6, IL-18, TSLP and MMP1 were highly expressed in the fibroblasts from SMG tissue of patients with IgG4-RD than in normal. The expression and secretion of IL-6 was greatly higher in IgG4-RD SMG fibroblasts than in normal. The expression and the secretion of IL-6 was upregulated by treatment with IL-1β, TNFα or TNFα/TGF-β. NF-κB inhibitor curcumin prevented the secretion and the expression of IL-6 induced by IL-1β or TNFα/TGF-β in the IgG4-RD SMG fibrobasts. Wnt1-inducible signaling protein 1 (WISP1) was also increased in the IgG4-RD SMG fibroblasts than in the normal. Curcumin also prevented WISP1 expression induced by IL-1β or TNFα/TGF-β in the normal. Treatment with IL-6 or WISP1 increased G2/M phase of the SMG fibroblasts in the normal. Expression of TSLP and IL-33 was increased in the IgG4-RD SMG fibroblasts than in the normal.
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Free Research Field |
耳鼻咽喉科学
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