| Project/Area Number |
23658265
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Clinical veterinary science
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| Research Institution | Osaka Prefecture University |
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Principal Investigator |
YAMATE Jyoji 大阪府立大学, 生命環境科学研究科(系), 教授 (50150115)
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| Co-Investigator(Kenkyū-buntansha) |
KUWAMURA Mitsuru 大阪府立大学, 生命環境科学研究科, 准教授 (20244668)
TAKANAKA Shigeo 大阪府立大学, 生命環境科学研究科, 准教授 (10280067)
IZAWA Takeshi 大阪府立大学, 生命環境科学研究科, 助教 (20580369)
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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 |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 上皮－間葉転換 / 線維化 / 尿細管上皮 / 胆管上皮 / 毛嚢上皮 / 体性幹細胞 / 毛根鞘細胞 / 幹細胞 / 平滑筋アクチン / PGE2 / 獣医病理学 / 萎縮腎 / 肝線維化 / betaーカテニン / α-平滑筋アクチン / EMT / 線維化腎 / 遡及現象 / ラット / 筋線維芽細胞 / 膵線維化 / Thy-1 |
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| Research Abstract |
Epithelial-mesenchymal transition (EMT) is a phenomenon in which injured epithelia acquire myofibroblastic properties, leading to progressive fibrosis. EMT was analyzed in renal epithelia, bile duct epithelia and follicular epithelia in renal fibrosis, peribiliary fibrosis and cutaneous fibrosis, respectively. The acquisition of myofibroblastic properties of incomplete renal regeneration in renal fibrosis was demonstrated; this EMT was inhibited by PGE2 and NGAL, but promoted by osteopontin. Since nephric blastema showed myofibroblastic properties, suggesting that renal EMT is a retroactive phenomenon towards renal blastema. Evident EMT was not shown in the bile duct epithelia in peribiliary fibrosis or follicular epithelia in cutaneous fibrosis. Myofibroblasts may be derived from the mesenchymal stem cells such as pericytes and bone-marrow stem cells. The present study gives a novel concept (EMT theory), which would open clues of possible therapies for intractable fibrosis.
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