| Project/Area Number |
21790764
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
OHTA Hiromitsu Tohoku University, 大学院・医学系研究科, 助教 (40451562)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 間質性肺炎 / 肺障害 / ARDSタイトジャンクション / 非閉塞性肺疾患 / 肺線維症 / タイトジャンクション |
|---|
| Research Abstract |
One of the pathological change of pneumonia, heart failure, and ARDS is thought to be a failure of barrier function of alveolar epithelial cells. We used bleomycin-induced pulmonary fibrosis model. After administration of bleomycin, expressions of tight junction-related proteins, especially claudin-5 and claudin-18 were down-regulated. We also analyzed the influence of transforming growth factor-β (TGF-β), a critical mediator of pulmonary fibrosis on tight junctions in vitro. The addition of TGF-β disrupted expressions of claudins. These results suggest that bleomycin-induced lung injury causes pathogenic alterations in tight junctions and that such alterations seem to be induced by TGF-β.
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