| Project/Area Number |
25461188
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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 | Nagoya University |
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Principal Investigator |
Ito Satoru 名古屋大学, 医学部附属病院, 病院講師 (60378073)
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| Co-Investigator(Kenkyū-buntansha) |
HASEGAWA Yoshinori 名古屋大学, 大学院医学系研究科, 教授 (20270986)
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| Co-Investigator(Renkei-kenkyūsha) |
Sokabe Masahiro 名古屋大学, 大学院医学系研究科, 特任教授 (10093428)
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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: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | メカニカルストレス / リモデリング / 気管支喘息 / 肺線維症 / カルシウムイオン / 気道平滑筋 / 肺線維芽細胞 / ATP / 細胞伸展 / 血管内皮 / 肺損傷 |
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| Outline of Final Research Achievements |
This study was designed to investigate effects of mechanical stress on cellular functions of airway smooth muscle cells and lung fibroblasts and the underlying mechanisms of mechanically induced cellular properties.
We found that ATP is released from airway smooth cells in response to mechanical stretch. We successfully visualized mechanically induced ATP releases from individual cells. ATP released from airway smooth muscle cells in response to mechanical stretch may regulate homeostasis of the airway physiology and play a role in the pathophysiology of asthma and COPD.
We also found that mechanical stretch activates the Ca2+ influx pathway independently of the actin cytoskeleton and released ATP in human lung fibroblasts. Our findings suggest that Ca2+ influx in response to mechanical stress would play a role in the progression of pulmonary fibrosis via activating lung fibroblasts.
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