| Project/Area Number |
15K10653
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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 |
Urology
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| Research Institution | Kansai University of Health Sciences |
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Principal Investigator |
Hatamura Ikuji 関西医療大学, 保健医療学部, 教授 (80336883)
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| Co-Investigator(Kenkyū-buntansha) |
伊藤 俊治 関西医療大学, 保健医療学部, 准教授 (50275351)
鍵弥 朋子 関西医療大学, 保健医療学部, 助教 (50717650)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | spermatogenesis / apoptosis / 精子形成 / アポトーシス / 無精子症 / 精子低分化 |
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| Outline of Final Research Achievements |
The spermatogenesis is one of the complex processes in mammalian body and the details have been unknown yet. At first, Kansl1-L was identified as a parathyroid gland specific gene in our early research. Kansl1-L targeted mice grew normally and kept health in their life. The tissue structure of the parathyroid gland of them was normal. The most evident feature of the Kansl1-L null mice was the male infertility. We investigated about causations of male infertility in Kansl1-L null mice. By our experiments, it was exhibited that Kansl1-L gene expressed strongly in spermatocyte of the seminiferous tubule. In Kansl1-L null mice, the size of testis was smaller than wild one. In addition, the expressions of some spermatocyte marker Hlf3 and Ccna1 genes were diminished and the spermatogenesis was stopped at the pachytene stage. As a result, apoptosis of spermatocytes was induced.This study was proved that Kansl1-L gene functioned as a key regulator of spermatogenesis.
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