Relationship of transcriptional markers to Leydig cell number in the mouse testis.

Diane Rebourcet,Sarah Smith,Laura Milne,Nathan Jeffery,Lee B Smith,Lyndsey Cruickshanks,Peter J O’Shaughnessy,Ana Monteiro

doi:10.1371/journal.pone.0219524

Abstract

ObjectivesThe current study aims to identify markers that would reflect the number of Leydig cells present in the testis, to help determine whether labour-intensive methods such as stereology are necessary. We used our well-characterised Sertoli cell ablation model in which we have empirically established the size of the Leydig cell population, to try to identify transcriptional biomarkers indicative of population size.ResultsFollowing characterisation of the Leydig cell population after Sertoli cell ablation in neonatal life or adulthood, we identified Hsd3b1 transcript levels as a potential indicator of Leydig cell number with utility for informing decision-making on whether to engage in time-consuming stereological cell counting analysis.

Highlights

Androgens are critical for male development, fertility and well-being [1,2,3,4]
Our group has recently shown that the Sertoli cells (SCs), key regulators of testis differentiation and adult spermatogenesis, control both the differentiation and development of the adult” Leydig cell (ALC) population in neonatal life, and their survival in adulthood [8, 9]
Postnatal retention of fetal-like-Leydig cells (LCs) is independent of SCs

Summary

Introduction

Androgens are critical for male development, fertility and well-being [1,2,3,4]. The principal source of androgens in the male are the testicular Leydig cells (LCs), which develop in two sequential waves or populations. A second “adult” Leydig cell (ALC) population starts to develop in the mouse at around 7–10 days [5,6,7]. These cells generate a pubertal surge of testosterone, which acts to promote and maintain adult fertility and to drive male reproductive behaviour. Our group has recently shown that the Sertoli cells (SCs), key regulators of testis differentiation and adult spermatogenesis, control both the differentiation and development of the ALC population in neonatal life, and their survival in adulthood [8, 9].

Objectives

Methods

Results