| Project/Area Number |
23591456
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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 |
膠原病・アレルギー・感染症内科学
|
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| Research Institution | University of Fukui (2012-2013)
Gunma University (2011) |
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Principal Investigator |
|
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| Co-Investigator(Kenkyū-buntansha) |
OKAJIMA Fumikazu 群馬大学, 生体調節研究所, 教授 (30142748)
HISADA Takeshi 群馬大学, 医学部, 講師 (10344938)
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| Project Period (FY) |
2011 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | プロトン / OGR1 / GPCR / 気道炎症 / 気管支喘息 / 樹状細胞 / 気管支平滑筋 / 気道リモデリング / CTGF / 気管支平滑筋細胞 / IL-8 / カルシウム / ERK / Gq / TNF |
|---|
| Research Abstract |
Ovarian cancer G protein-coupled receptor 1 (OGR1) stimulation by extracellular protons causes the activation of G proteins and subsequent cellular functions. We showed that OGR1-deficient mice are resistant to the cardinal features of asthma, including airway eosinophilia, airway hyperresponsiveness, and goblet cell metaplasia in a murine allergic asthma model. On the other hand, acidic pH alone induced a substantial production of connective tissue growth factor (CTGF) and enhanced transforming growth factor-beta-induced CTGF mRNA and protein expression through OGR1 in human airway smooth muscle cells. Our results suggest that OGR1 plays an important role in the pathogenesis of allergic airway inflammtion and airway remodelling and OGR1 may be a therapeutic target of asthma.
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