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Title: The Luteinizing Hormone-Testosterone Pathway Regulates Mouse Spermatogonial Stem Cell Self-Renewal by Suppressing WNT5A Expression in Sertoli Cells
Authors: Tanaka, Takashi
Kanatsu-Shinohara, Mito
Lei, Zhenmin
Rao, C.V.
Shinohara, Takashi
Author's alias: 田中, 敬
篠原, 美都
篠原, 隆司
Issue Date: 9-Aug-2016
Publisher: Elsevier Inc.
Journal title: Stem Cell Reports
Volume: 7
Issue: 2
Start page: 279
End page: 291
Abstract: Spermatogenesis originates from self-renewal of spermatogonial stem cells (SSCs). Previous studies have reported conflicting roles of gonadotropic pituitary hormones in SSC self-renewal. Here, we explored the role of hormonal regulation of SSCs using Fshb and Lhcgr knockout (KO) mice. Although follicle-stimulating hormone (FSH) is thought to promote self-renewal by glial cell line-derived neurotrophic factor (GDNF), no abnormalities were found in SSCs and their microenvironment. In contrast, SSCs were enriched in Lhcgr-deficient mice. Moreover, wild-type SSCs transplanted into Lhcgr-deficient mice showed enhanced self-renewal. Microarray analysis revealed that Lhcgr-deficient testes have enhanced WNT5A expression in Sertoli cells, which showed an immature phenotype. Since WNT5A was upregulated by anti-androgen treatment, testosterone produced by luteinizing hormone (LH) is required for Sertoli cell maturation. WNT5A promoted SSC activity both in vitro and in vivo. Therefore, FSH is not responsible for GDNF regulation, while LH negatively regulates SSC self-renewal by suppressing WNT5A via testosterone.
Description: 精子幹細胞の自己複製を促す新規遺伝子の発見. 京都大学プレスリリース. 2016-08-10.
Rights: © 2016 The Author(s). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
URI: http://hdl.handle.net/2433/216286
DOI(Published Version): 10.1016/j.stemcr.2016.07.005
PubMed ID: 27509137
Related Link: https://www.kyoto-u.ac.jp/ja/research-news/2016-08-10-0
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