Nongenomic activation of spermatozoa by steroid hormones: Facts and fictions

Abstract

a b s t r a c tThe rapid effects of steroids on spermatozoa have been demonstrated for the first time two decades ago. Progesterone (P), which is present throughout the female genital tract with peaks of levels in the cumulus matrix surrounding the oocyte, stimulates several sperm functions, including hyperactivation and acrosome reaction. These effects are mediated by an extranuclear pathway, as P stimulates an influx of calcium, the tyrosine phosphorylation of sperm proteins and other signalling cascades in a rapid manner. Whether these effects are receptor mediated and which receptors mediate these effects are still a matter of discussion despite all the efforts of the scientific community aimed at identifying them during the last 20 years. Although responsiveness to P is related to sperm fertilizing ability, the physiological role of P during the process of fertilization is discussed, and recent evidence points for a role of the steroid as a chemotactic agent for sperm. A similar situation applies for estrogens (E), which have been shown to induce direct effects on sperm by an extranuclear pathway. In particular, E appear to decrease acrosome reaction in response to P, exerting a role in ensuring an appropriate timing for sperm exocytosis during the process of fertilization.

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

“…Estrogens play a key role during male reproduction including spermatogenesis (Carreau et al 2011(Carreau et al , 2012 and sperm maturation such as capacitation (Baldi et al 2009). Estrogen response is mediated through both genomic and non-genomic actions, where the genomic one involves binding to estrogen receptors ERs and nuclear transcription factors that activate the expression of target genes.…”

Suppression of progesterone-enhanced hyperactivation in hamster spermatozoa by estrogen

“…Calcium is a key molecule in the regulation of AR and hyperactivation by steroid hormones (Luconi et al 1999, Baldi et al 2000, 2009, Noguchi et al 2008, Fujinoki 2009). After progesterone binds to the sperm head, it stimulates calcium influx and activation of PLC (Fukami et al 2003, Lö sel & Wehling 2003, Harper et al 2004, Luconi et al 2004, Noguchi et al 2008, Baldi et al 2009, Fujinoki 2009). Moreover, spermatozoa are not hyperactivated in the mTALP medium without calcium (Fujinoki 2008, Noguchi et al 2008.…”

“…Progesterone stimulates the AR via non-genomic regulation (Baldi et al 1998, 2009, Lö sel & Wehling 2003, Luconi et al 2004. In human spermatozoa, progesterone stimulates calcium influx, tyrosine phosphorylation, chloride efflux, and cAMP increase (Lösel & Wehling 2003, Harper et al 2004, Luconi et al 2004, Baldi et al 2009). It also stimulates ZP penetration and the AR in hamster spermatozoa (Libersky & Boatman 1995b, Llanos & Anabalon 1996.…”

“…Estrogen receptors (ESRs) are also present in the cell membrane (Luconi et al 1999, Baldi et al 2000, 2009. Moreover, the suppression of progesterone-induced AR by 17bE 2 is non-genomic (Luconi et al 2004, Baldi et al 2009.…”

Fluorescence Technique Description for Measuring Ca<sup>2+</sup> in Mice Sperm

“…Spermatozoa produce Ca 2+ signals in response to extracellular changes, for instance ZP induced acrosome reaction, chemotaxis in response to low dose progesterone [1] [6]. During capacitation, hyperactivation and the acrosome reaction there is evidence for increasing Ca 2+ concentration in several mammalian species including human [11] [12]. Sperm have many channels on cell membrane provoke Ca 2+ influxes and internal release of Ca 2+ through these channels.…”