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Hydroxysteroid (17 beta) dehydrogenase 1 expressed by Sertoli cells contributes to steroid synthesis and is required for male fertility

Journal article
Authors J. Hakkarainen
F. P. Zhang
H. Jokela
A. Mayerhofer
R. Behr
S. Cisneros-Montalvo
Mirja Nurmio
Jorma Toppari
Claes Ohlsson
N. Kotaja
P. Sipila
Matti Poutanen
Published in Faseb Journal
Volume 32
Issue 6
Pages 3229-3241
ISSN 0892-6638
Publication year 2018
Published at Institute of Medicine
Pages 3229-3241
Language en
Links dx.doi.org/10.1096/fj.201700921R
Keywords HSD17B1, infertility, spermatogenesis, cell junctions, mullerian-inhibiting substance, follicle-stimulating-hormone, 17-beta-hydroxysteroid-dehydrogenase type-1, luteinizing-hormone, ectoplasmic specialization, in-vivo, seminiferous epithelium, estradiol, production, sexual development, male-infertility, Biochemistry & Molecular Biology
Subject categories Clinical Medicine

Abstract

The pituitary gonadotrophins and testosterone are the main hormonal regulators of spermatogenesis, but estradiol is also known to play a role in the process. The hormonal responses in the testis are partially mediated by somatic Sertoli cells that provide nutritional and physical support for differentiating male germ cells. Hydroxysteroid (17 beta) dehydrogenase 1 (HSD17B1) is a steroidogenic enzyme that especially catalyzes the conversion of low potent 17keto-steroids to highly potent 17 beta-hydroxysteroids. In this study, we show that Hsd17b1 is highly expressed in Sertoli cells of fetal and newborn mice, and HSD17B1 knockout males present with disrupted spermatogenesis with major defects, particularly in the head shape of elongating spermatids. The cell-cell junctions between Sertoli cells and germ cells were disrupted in the HSD17B1 knockout mice. This resulted in complications in the orientation of elongating spermatids in the seminiferous epithelium, reduced sperm production, and morphologically abnormal spermatozoa. We also showed that the Sertoli cell-expressed HSD17B1 participates in testicular steroid synthesis, evidenced by a compensatory up-regulation of HSD17B3 in Leydig cells. These results revealed a novel role for HSD17B1 in the control of spermatogenesis and male fertility, and that Sertoli cells significantly contribute to steroid synthesis in the testis.

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