| Project/Area Number |
23591171
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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 | Fukuoka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
UCHINO Junji 福岡大学, 医学部, 講師 (80432946)
田代 尚樹 福岡大学, 医学部, 助教 (70613884)
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| Co-Investigator(Renkei-kenkyūsha) |
TASHIRO Naoki 福岡大学, 医学部, 助教 (70613884)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 肺線維症 / HB-EGF / ＨＢ－ＥＧＦ |
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| Research Abstract |
The aim of this study is to clarify the role of HB-EGF in respiratory diseases, especially pulmonary fibrosis and to develop new remedy for pulmonary fibrosis.
The expression of HB-EGF was elevated in the bleomycin induced pulmonary fibrosis in inflammation phase. Then the expression was decreased in fibrosis phase. The HB-EGF expression was down-regulated in clinical specimen from the idiopathic pulmonary fibrosis. Therefore, it was revealed that the expression of HB-EGF was down-regulated related to pulmonary fibrosis. We hypothesized that overexpression of HB-EGF might lead to rescue of pulmonary fibrosis. We administered of adenovirus vector of HB-EGF expression or recombinant HB-EGF into bleomycin induced pulmonary fibrosis model. However, the apparent attenuation was not attained. As a result, the expression of HB-EGF was down-regulated in pulmonary fibrosis, but overexpression of HB-EGF did not result in attenuation of pulmonary fibrosis in this study.
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