| Project/Area Number |
23590169
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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 |
Medical pharmacy
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| Research Institution | Akita University |
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Principal Investigator |
OYAMADA Hajime 秋田大学, 医学部, 臨床検査技師長 (80375310)
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| Co-Investigator(Kenkyū-buntansha) |
MORITOKI Yuki 秋田大学, 医学部, 講師 (90585522)
CHIHARA Junichi 蘇生会病院, 名誉理事 (80197615)
UEKI Shigeharu 秋田大学, 医学部, 准教授 (60361234)
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| Project Period (FY) |
2011 – 2013
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| 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: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | プロスタグランジンD2 / PGD2受容体 / ケモカイン受容体CCR3 / アレルギー炎症 / DP / CRTH2 / CCR3 / GPER / PGD2 / 気道上皮細胞 / 好酸球 |
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| Research Abstract |
Prostaglandin D2 (PGD2) has been known to play an important role in allergic inflammation through cell surface receptor CRTH2 and DP1, and also through nuclear receptor PPARg. Our previous study suggested the presence of novel receptor other than these three known receptors for PGD2.
Since we found that PGD2 induced chemokine receptor CCR3 internalization, we studied the possibility that PGD2 act through CCR3. Receptor binding assay and calcium signaling assay using CCR3-transfected cell indicated that PGD2 did not bind/activate CCR3.
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