| Project/Area Number |
25461192
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kumamoto University |
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Principal Investigator |
Endo Motoyoshi 熊本大学, 大学院生命科学研究部, 助教 (40398243)
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| Co-Investigator(Renkei-kenkyūsha) |
INOUE Hiromasa 鹿児島大学, 大学院医歯学総合研究科, 教授 (30264039)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 間質性肺炎 / Angptl2 / ブレオマイシン肺臓炎 / 肺線維症 / ブレオマイシン / マクロファージ |
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| Outline of Final Research Achievements |
Idiopathic pulmonary fibrosis is defined as progressive interstitial pneumonia with poor prognosis. However, the mechanism of it remains unclear. Angiopoietin-like protein 2 (Angptl2) is a chronic inflammatory mediator, which when deregulated is associated with various pathologies. However, little was known about its potential lung function. To examine the role of Angptl2 for lung function, we generated a rabbit monoclonal antibody that specifically recognizes mouse Angptl2 and then evaluated protein expression in mouse lung tissue. We observed abundant Angptl2 expression in both alveolar epithelial type I and type II cells and in alveolar macrophages under normal conditions. Next, we examined Angptl2 lung function in a mouse interstitial pneumonia model and found that Angptl2 deficiency made fibrosis caused by bleomycin exacerbated fibrosis. Overall, our findings suggest that Angptl2 expression in lung epithelial cells may function in repair of damaged tissue.
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