Kyoto University-led finding point to male infertility treatment
Spermatogonial stem cells make sperm throughout a man's life, but what if they don't work?
Kyoto University researchers and collaborators may be approaching a remedy. In a recent study, the scientists have announced finding a new gene that enhances self-replication of spermatogonial stem cells.
The newly-discovered gene, Wnt5a, become inactive in response to lutenizing horomones, which signal certain cells to produce testosterone. In humans, Wnt5a also controls signals related to cell development and cancer.
"This came as a surprise, because the assumption in the field was that follicle stimulating hormones and not lutenizing hormones promoted sperm production," says study author Takashi Shinohara.
The rarity of spermatogonial stem cells pose significant challenges to their study, as they constitute only 0.02-0.03% of all testicular cells. In addition, they have no unique molecular markers. To surmount these obstacles, the team transplanted spermatogonial stem cells into sterile mice to track how they would proliferate.
"The current culturing technique for spermatogonial stem cells is used in mice, rats, and hamsters," says Shinohara. "But the Wnt5a gene should be useful for culturing spermatogonial cells of other animals, including humans. We hope that further refinement of the technique will contribute to developing treatments for male infertility."
Lutenizing hormones inhibit Wnt5a expression and spermatogonial cell replication
Paper Information
【DOI】 http://dx.doi.org/10.1016/j.stemcr.2016.07.005
【KURENAI Access URL】 http://hdl.handle.net/2433/216286
Takashi Tanaka, Mito Kanatsu-Shinohara, Zhenmin Lei, C.V. Rao and Takashi Shinohara. (2016). The Luteinizing Hormone-Testosterone Pathway Regulates Mouse Spermatogonial Stem Cell Self-Renewal by Suppressing WNT5A Expression in Sertoli Cells. Stem Cell Reports, 7(2), pp. 279–291.
