| Project/Area Number |
23591451
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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 |
膠原病・アレルギー・感染症内科学
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KOHNO Kimitoshi 産業医科大学, 医学部, 名誉教授 (00153479)
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| Co-Investigator(Renkei-kenkyūsha) |
TANAKA Yoshiya 産業医科大学, 医学部, 教授 (30248562)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | リモデリング抑制 / Wnt10 / 膠原病 |
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| Research Abstract |
The aim of this study is to elucidate the mechanism of EMT and EndoMT in tissue remolding and fibrosis of rheumatic diseases and to develop a new treatment strategy for rheumatic diseases. We conducted immune-staining of skin,lung and kidney tissue from rheumatic disease including rheumatoid arthritis, systemic sclerosis and vasculitis. As a result, a hyperplasia of myofibroblast was observed at the site of prominent progression of tissue fibrosis and vascular remodeling due to endothelial dell proliferation. Immuno-staining revealed both the myoblast and endothelial cells express Wnt10a, suggesting signaling through Wnt10 might involvement in irreversible remodeling in rheumatic diseases. These provocative findings suggest that the inhibition of EndMT/EMT may be a promising target for clinical therapeutic translation in settings such as tissue remodeling which cause of irreversible organ damage in rheumatic deseases.
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