Abstract
Oestrogen is an important regulator in reproduction. To understand the role of oestrogen receptor 1 (ESR1) in Leydig cells, we investigated the expression of ESR1 in mouse Leydig cells during postnatal development and the effects of oestrogen on steroidogenesis and proliferation of progenitor Leydig cells (PLCs). In Leydig cells, the ESR1 expression was low at birth, increased until postnatal day 14 at which PLCs were predominant, and then decreased until adulthood. In foetal Leydig cells, ESR1 immunoreactivity increased from birth to postnatal day 14. These suggest that ESR1 is a potential biomarker of Leydig cell development. In PLCs, 17β-estradiol and the ESR1-selective agonist propylpyrazoletriol suppressed human chorionic gonadotropin (hCG)-induced progesterone production and steroidogenic gene expression. The ESR2-selective agonist diarylpropionitrile did not affect steroidogenesis. In PLCs from Esr1 knockout mice, hCG-stimulated steroidogenesis was not suppressed by 17β-estradiol, suggesting that oestrogen inhibits PLC steroidogenesis via ESR1. 17β-estradiol, propylpyrazoletriol, and diarylpropionitrile decreased bromodeoxyuridine uptake in PLCs in the neonatal mice. In cultured PLCs, 17β-estradiol, propylpyrazoletriol, and diarylpropionitrile reduced hCG-stimulated Ki67 and Pcna mRNA expression and the number of KI67-positive PLCs, suggesting that oestrogen inhibits PLC proliferation via both ESR1 and ESR2. In PLCs, ESR1 mediates the oestrogen-induced negative regulation of steroidogenesis and proliferation.
Highlights
Participates in Leydig cell development and in the maintenance of a stable Leydig cell population by regulating progenitor Leydig cells (PLCs) and adult Leydig cells (ALCs) proliferation
We investigated the expression of ESR1 during the postnatal development of Leydig cells and the role of ESR1 in steroidogenesis and proliferation of PLCs in the mouse testes
In both seminiferous tubules and interstitial cells, the Esr[1] mRNA level increased from postnatal day (PND) 7 to 14 and decreased thereafter. This result indicated that the observation of maximal ESR1 protein expression in the testis at PND 7 is due to the presence of fewer seminiferous tubular cells relative to PND 14
Summary
Participates in Leydig cell development and in the maintenance of a stable Leydig cell population by regulating PLC and ALC proliferation. The two oestrogen receptor isoforms, ESR1 and ESR2, are known to mediate the genomic action of oestrogen Both oestrogen receptor subtypes are present in male reproductive organs[20]. In adult rat Leydig cells, endogenous oestrogen inhibits the activities of steroidogenic enzymes via ESR1 action[33]. These suggest the participation of ESR1 in ALC function. At present, neither the expression pattern of ESR1 throughout ALC development nor the role of oestrogen receptor signalling in PLC steroidogenesis and proliferation is well understood. We investigated the expression of ESR1 during the postnatal development of Leydig cells and the role of ESR1 in steroidogenesis and proliferation of PLCs in the mouse testes
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
