| Project/Area Number |
24591138
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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 | Dokkyo Medical University |
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Principal Investigator |
TO Masako 獨協医科大学, 医学部, 准教授 (90595597)
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| Co-Investigator(Renkei-kenkyūsha) |
HARUKI Kosuke 獨協医科大学, 医学部, 教授 (30286421)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | HIF-1α / 肺気腫 / 慢性閉塞性肺疾患 / ＶＥＧＦ |
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| Outline of Final Research Achievements |
We have previously reported that HIF-1α and HDAC7 levels in nuclei under hypoxia condition were lower in COPD compared to control subjects. In this project, we investigated the association between this findings and the progression of emphysema in COPD patients.
In HDAC7 knockdown cells, HIF-1α nuclear translocation and subsequent VEGF expression were suppressed compares to control cells. Hypoxia induced- cytokine and protease expressions were HIF-1α independent and NF-kB p65 dependent. Hypoxia induced- cytokine and protease expressions were not suppressed in HDAC7 knockdown cells. The abnormal response to hypoxia in COPD patients seems to be a one of the factors for the progression of emphysema due to the depression of VEGF and the increase of inflammatory cytokines and proteases.
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