| Project/Area Number |
26860597
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | 独立行政法人国立病院機構高崎総合医療センター(臨床研究部) |
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Principal Investigator |
Manabu Ueno 独立行政法人国立病院機構高崎総合医療センター(臨床研究部), 臨床研究部, 呼吸器内科医長 (70599563)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 慢性閉塞性肺疾患 / 肺気腫 / マクロファージ / テロメラーゼ / テロメア |
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| Outline of Final Research Achievements |
Chronic Obstructive Pulmonary Disease(COPD) is characterized as persistent inflammation centering on the alveolar macrophages caused by the cigarette smoking. In this study, we analysed the telomerase of alveolar cells in COPD and examined the involvement of chronic inflammation.
In smoking-induced emphysema mice, the telomerase activity was increased alveolar macrophages and telomere shortening was suppressed. Whereas, the telomerase of alveolar type II cells was suppressed. Moreover, TERT expression was increased in alveolar macrophages. By smoking, the telomerase activity of alveolar macrophages was confirmed to prolong the cell life and was considered to be a contributing factor for chronic persistent inflammation in COPD.
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