| Project/Area Number |
09670620
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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 | KYUSHU UNIVERSITY |
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Principal Investigator |
KUWANO Kazuyoshi KYUSHU UNIVERSITY, Faculty of Med, Ass.Prof., 医学部・附属病院, 講師 (40205266)
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| Co-Investigator(Kenkyū-buntansha) |
HAGIMOTO Naoki KYUSHU UNIVERSITY , Faculty of Med, Ass.Prof., 大学院・医学研究院, 助手 (50315074)
川崎 雅之 九州大学, 大学院・医学系研究科, 助手 (90264051)
田中 拓夫 九州大学, 医学部, 医員
金子 由美 九州大学, 医学部, 医員
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| Project Period (FY) |
1997 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2000: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1999: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | lung injury / pulmonary fibrosis / apoptosis / Fas抗原 / Fasリガンド / カスパーゼ |
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| Research Abstract |
Pulmonary fibrosis caused by tissue remodeling consisting of fibroblast proliferation, which is induced by bronchiolar and alveolar epithelial cell damage and prolongation of inflammation. We have examined the hypothesis that apoptosis of inflammatory cells and lung epithelial cells may be involved in this process. We described the abstract below. 1) DNA damage and p53 and p21 overexpression in lung epithelial cells from patients with IPF 2) Fas and FasL upregulation in lung epithelial cells and infiltrating lymphocytes, respectively, in lung epithelial cells from patients with IPF 3) Upregulation of p53, Fas, FasL in bleomycin-induced pneumopathy 4) Pulmonary fibrosis induced by inhalation of agonistic anti-Fas antibody 5) Fas- or FasL-deficient mice are resistant against bleomycin-induced pneumopathy 6) Amelioration of LPS- or bleomycin induced pneumopathy in mice by a caspase inhibitor
These results suggest that lung epithelial cell apoptosis is involved in the pathophysiology of pulmonary fibrosis.
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