2014 Fiscal Year Final Research Report
Analysis of the role of cyclooxygenase 2 on spermatogenesis disturbance.
Project/Area Number |
24592449
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Urology
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Research Institution | Nagoya City University |
Principal Investigator |
KUBOTA Hiroki 名古屋市立大学, 医学(系)研究科(研究院), 研究員 (10347403)
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Co-Investigator(Kenkyū-buntansha) |
KOHRI Kenjiro 名古屋市立大学, その他の部局, 学長 (30122047)
HAYASHI Yutaro 名古屋市立大学, 大学院医学研究科, 准教授 (40238134)
SASAKI Shoichi 名古屋市立大学, 大学院医学研究科, 准教授 (50225869)
UMEMOTO Yukihiro 名古屋市立大学, 大学院医学研究科, 講師 (80381812)
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Research Collaborator |
PARRINGTON John Oxford大学
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | Cyclooxygenase2 / Spermatogenesis |
Outline of Final Research Achievements |
In this study, we examined whether COX-2 was induced in impaired testes, and also investigated the possible role of COX in the testes using experimental cryptorchidism model mice. Five-week-old male mice underwent an operation to induce unilateral cryptorchidism, and they were then divided into three groups. Immunohistological staining and RT-PCR revealed that the expression of COX-2 was increased in the experimental cryptorchid testes. TdT-mediated dUTP-biotin nick end-labeling (TUNEL) staining revealed that the number of apoptotic cells was significantly increased by COX-2 inhibitor. However, the COX-1 inhibitor did not appear to affect spermatogenesis in the experimental cryptorchid testes. These results suggest that the COX-2 inhibitor provoked testicular damage in experimental cryptorchidism by inducing germ cell apoptosis. The expression of COX-2 might be induced to protect germ cells from heat stress caused by experimental cryptorchidism.
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Free Research Field |
アンドロロジー
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