2010 Fiscal Year Final Research Report
Investigation of mechanism of acute exacerbation of interstitial pneumonia. Alveolar barrier dysfunction was observed in fibrotic lung
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 |
Research Field |
Respiratory organ internal medicine
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Research Institution | Tohoku University |
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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Keywords | 間質性肺炎 / 肺障害 / ARDS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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[Journal Article] Gradual increase of high mobility group protein B1 (HMGB1) in the lungs after the onset of acute exacerbation of idiopathic pulmonary fibrosis.2011
Author(s)
Ebina M, Taniguchi H, Miyasho T, Yamada S, Shibata N, Ohta H, Hisata S, Hirota N, Nishimura H, Ishizaka A, Maruyama I, Takashi K, Nukiwa T.
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Journal Title
Pulmonary Medicine
Pages: 1-9
Peer Reviewed
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[Remarks] ホームページ等