| Project/Area Number |
26860743
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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 |
Collagenous pathology/Allergology
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| Research Institution | Akita University |
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Principal Investigator |
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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: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | アレルギー / 喘息 / GPR30 / エストロゲン / 性差 / 好酸球 / エスロトゲン / 受容体 / GRP30 |
|---|
| Outline of Final Research Achievements |
We investigated the role of GPR30, one of estrogen receptor, in the pathogenesis of asthma. We revealed that administration of G-1, GPR30-specific agonist, attenuated airway inflammatory cell accumulation and airway hyperresponsiveness in OVA-sensitized and OVA-challenged mice. On the other hand, these responses were not induced in IL-10-deficient mice. These results indicate that extended GPR30 activation negatively regulates the acute asthmatic condition by altering IL-10 producing lymphocyte population.
In addition, we investigate the role of G-1 in human eosinophil function. We revealed that administration of G-1 inhibited eosinophil spontaneous apoptosis in absence of IL-5. In contrast, G-1 induced apoptosis when human eosinophils were co-stimulated with IL-5. These results indicate that GPR30 plays an important role in the pathogenesis of asthma.
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