Analysis of crosstalk between epididymal and prostatic epithelial cells in male infertile mice
Project/Area Number |
17K08493
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General anatomy (including histology/embryology)
|
Research Institution | Kumamoto University |
Principal Investigator |
YOSHINAGA Kazuya 熊本大学, 大学院生命科学研究部(保), 教授 (50136719)
|
Co-Investigator(Kenkyū-buntansha) |
竹田 直樹 熊本大学, 生命資源研究・支援センター, 助教 (90304998)
|
Project Period (FY) |
2017-04-01 – 2020-03-31
|
Project Status |
Completed (Fiscal Year 2019)
|
Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | 細胞・組織 / 発生・分化 / 上皮・間葉間相互作用 / 男性生殖器 / 雄性生殖管 / マウス |
Outline of Final Research Achievements |
The present study showed that in LGR4 hypomorphic mutant mice, the elongation and bending of the male reproductive tract were impaired during the late embryonic and juvenile periods. In addition, LGR4 expression was mainly observed in peritubular mesenchymal cells, and the proliferation of epithelial cells and peripheral mesenchymal cells that compose the male reproductive tract of mutant mice was decreased from embryonic day 14.5. During this period, apoptosis of mesenchymal cells was increased. These results indicate that LGR4 and epithelial-mesenchymal interactions are important for the development and differentiation of the male reproductive tract.
|
Academic Significance and Societal Importance of the Research Achievements |
精巣上体や前立腺を構成する細胞の発生・分化や細胞間調節機構の仕組みはよく分かっていない。本研究は、細胞内シグナル伝達に関与する受容体LGR4が雄性生殖管の形態形成期における細胞増殖を促進することを示し、その発生・分化を制御する分子メカニズムの一端を明らかにした。この成果は今後、男性不妊症の原因解明や診断・治療法の開発のみならず、さまざまな上皮性器官の形態形成異常を伴う疾患の原因解明にも繋がることが期待される。
|
Report
(4 results)
Research Products
(4 results)