| Project/Area Number |
25462565
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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 |
Obstetrics and gynecology
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| Research Institution | Oita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NARAHARA HISASHI 大分大学, 医学部産科婦人科, 教授 (60211447)
NASU KAEI 大分大学, 医学部地域医療支援システム産婦人科分野, 教授 (30274757)
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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: ¥260,000 (Direct Cost: ¥200,000、Indirect Cost: ¥60,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | 子宮内膜 / 着床 / PAR |
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| Outline of Final Research Achievements |
To investigate the effect of sperm on endometrial function, the kinase activation via protease-activated receptor (PAR)-2 in endothelial epithelial cells (EECs) and endometrial stromal cells (ESCs) were investigated. Following stimulation by sperm and the PAR-2 agonist, the mitogen-activated protein kinase (MAPK) activity such as extracellular signal-regulated kinase (ERK)-1/2, p38, c-Jun N-terminal kinase (JNK), and glycogen synthase kinase (GSK)-3 were activated, and these signals were inhibited by the PAR-2 antagonist. From our data, the results suggest that sperm induces activation of the MAPK system via PAR-2, leading to the modulation of endometrial function.
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