| Project/Area Number |
21590979
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Hokkaido University |
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Principal Investigator |
TANINO Mishie 北海道大学, 大学院・医学研究科, 助教 (90360908)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Shinya 北海道大学, 大学院・医学研究科, 教授 (70261287)
BETSUYAKU Tomoko 北海道大学, 大学院・医学研究科, 准教授 (60333605)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 特発性肺線維症 / アダプター分子 / CRK / 上皮間葉移行 / アダプター蛋白 / 肺胞上皮細胞 / 線維芽細胞 |
|---|
| Research Abstract |
Idiopathic pulmonary fibrosis (IPF) is chronic, progressive, and fibrosing lung disease and there is no advantageous drug for longer survival in IPF patients. Recently, involvement of epithelial mesenchymal transition (EMT) is suggested as one of the pathogenesis of IPF. In this study, we have demonstrated CRKI/II is highly expressed in alveolar type II (AT II) cells in IPF/UIP specimens and CRK II overexpressed A549 cell line could be induced stronger EMT phenomenon under TGF-β1 stimulation. These results suggested suppression of CRK II in ATIIcells might be one of the therapeutic strategy for regulating lung fibrosis in IPF/UIP by regulation of EMT.
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