Pathophysiologic mechanisms underlying emphysema and osteoporosis
| Project/Area Number |
26860617
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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 | Keio University |
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Principal Investigator |
Sasaki Mamoru 慶應義塾大学, 医学部, 助教 (90573311)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 慢性閉塞性肺疾患 / 骨粗鬆症 / 喫煙曝露 / マウス / 骨代謝 / 骨強度 / 骨質 / 肺気腫 / 骨密度 |
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| Outline of Final Research Achievements |
The pathophysiologic mechanisms underlying emphysema and osteoporosis have not been fully elucidated. The aim of this study is to determine the effects of short- and long-term cigarette smoke (CS) exposure on bone metabolism, structure and histological changes in a mouse model of CS-induced emphysema. And we examined the effects of cigarette smoke extract (CSE) on the osteoclast-like cell in vitro.
In vivo, both bone resorption and formation markers were significantly decreased in short-term CS-exposed mice. However, those are inversely increased in long-term CS-exposed mice compared to air controls, implying a dynamic shift of bone metabolism from low- toward high-turnover. Bone volume of CS-exposed mice was increased, but bone histomorphometric analysis revealed the increase of osteoclasts. In vitro, CSE directly impaired the differentiation of osteoclast-like cells, this findings partly explain a phenomenon observed in vivo short-term CS exposed mice.
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Report
(3 results)
Research Products
(5 results)
