Abstract
High 17β-Estradiol (E2) levels are known to cause alterations of spermatogenesis and environments throughout the male reproductive tract. Sertoli cells (SCs) ensure an adequate environment inside the seminiferous tubule. Glycerol stands as essential for the maintenance of blood–testis barrier created by SCs, however, the role of E2 in this process is not known. Herein, we hypothesized that the effect of E2 on glycerol permeability in mouse SCs (mSCs) could be mediated by aquaglyceroporins. The expression of aquaglyceroporins was assessed by RT-PCR and qRT-PCR. Glycerol permeability was evaluated by stopped-flow light scattering. We were able to identify the expression of AQP3 and AQP9 in mSCs where AQP9 is more abundant than AQP3. Our results show that high E2 levels decrease AQP9 mRNA abundance with no influence on AQP3 in mSCs. Interestingly, high E2 levels decreased mSCs’ permeability to glycerol, while downregulating AQP9 expression, thus suggesting a novel mechanism by which E2 modulates fluid secretion in the testis. In conclusion, E2 is an important regulator of mSCs physiology and secretion through changes in AQP9 expression and function. Thus, alterations in glycerol permeability induced by E2 may be the cause for male infertility in cases associated with the presence of high E2 levels.
Highlights
In the last two decades, extensive research showed that beyond the classic view on the major relevance of androgens for male reproduction, estrogens can regulate the development and function of the male reproductive tract. 17β-Estradiol (E2) is found in measurable concentrations in the blood of men and higher concentrations have been reported in the testis and semen [1,2]
We were able to identify the expression of Aqp3 and Aqp9, but the presence of Aqp7 was not detected in mouse SCs (mSCs) (Figure 1A)
The role of estrogens in male reproductive function has been exhaustively investigated in the last decades, providing evidence that estrogens are crucial to the establishment of male reproductive potential [3,23,24]
Summary
In the last two decades, extensive research showed that beyond the classic view on the major relevance of androgens for male reproduction, estrogens can regulate the development and function of the male reproductive tract. 17β-Estradiol (E2) is found in measurable concentrations in the blood of men and higher concentrations have been reported in the testis and semen [1,2]. E2 is necessary for the healthy development and function of the male reproductive organs. Elevated levels of this hormone induce deleterious effects that are consistently associated with male. Elevated E2 levels induce morphological alterations in Sertoli cells (SCs) and Leydig cells that result in severe failures in spermatogenesis [4]. High E2 levels change ionic homeostasis and the transport of some molecules within the seminiferous tubule, and some of those molecules may alter or even arrest spermatogenesis. Elevated concentrations of glycerol in testis causes changes in the function of the blood–testis barrier (BTB), compromising the homeostasis of the tubular fluid and leading to the death of germ cells [5]. Chronic exposure to high glycerol concentrations may prompt permanent oligospermia or even azoospermia [5]. SCs are responsible for the maintenance of the BTB [8] and for promoting normal spermatogenesis
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