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NEDD4促进小鼠睾丸中支持细胞增殖和成年睾丸间质细胞分化。

NEDD4 Promotes Sertoli Cell Proliferation and Adult Leydig Cell Differentiation in the Murine Testis.

作者信息

Windley Simon Peter, Neirijnck Yasmine, Vidovic Diana, Schwarz Quenten, Kumar Sharad, Nef Serge, Wilhelm Dagmar

机构信息

Department of Anatomy & Physiology, The University of Melbourne, Parkville 3100, Australia.

Department of Biochemistry and Molecular Biology, Monash Biomedicine Discovery Institute, Monash University, Melbourne 3800, Australia.

出版信息

Endocrinology. 2025 Jul 8;166(9). doi: 10.1210/endocr/bqaf115.

Abstract

Successful testis development relies on the coordinated differentiation and assembly of various cell types to establish both endocrine and reproductive functions. The ubiquitin ligase NEDD4 has emerged as a key player in murine testis development, with this enzyme being implicated in gonadal sex determination and spermatogonial stem cell differentiation. Here, we report hitherto uncharacterized roles of NEDD4 in postnatal testis development. Utilizing Nr5a1- and Amh-Cre drivers to conditionally ablate Nedd4 in testicular somatic cells, we show that NEDD4 promotes Sertoli cell proliferation through the modulation of the PI3K-AKT signaling pathway. This ubiquitin ligase also ensures proper differentiation of adult Leydig cells and may contribute to murine steroidogenesis. Furthermore, NEDD4 is essential for adrenal gland differentiation, as its loss results in adrenal dysgenesis. These findings highlight NEDD4 as a crucial factor in testis development, emphasizing the importance of ubiquitination and post-translational modifications in reproductive biology.

摘要

成功的睾丸发育依赖于各种细胞类型的协调分化和组装,以建立内分泌和生殖功能。泛素连接酶NEDD4已成为小鼠睾丸发育中的关键角色,该酶与性腺性别决定和精原干细胞分化有关。在此,我们报告了NEDD4在出生后睾丸发育中迄今未被描述的作用。利用Nr5a1和Amh-Cre驱动因子有条件地在睾丸体细胞中敲除Nedd4,我们发现NEDD4通过调节PI3K-AKT信号通路促进支持细胞增殖。这种泛素连接酶还确保成年睾丸间质细胞的正常分化,并可能有助于小鼠的类固醇生成。此外,NEDD4对肾上腺分化至关重要,因为其缺失会导致肾上腺发育不全。这些发现突出了NEDD4作为睾丸发育中的关键因素,强调了泛素化和翻译后修饰在生殖生物学中的重要性。

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