Progesterone and RU486: opposing effects on human sperm.

Yang, Jing; Serres, Catherine; Philibert, D.; Röbel, P; Baulieu, Étienne-Émile; Jouannet, Pierre

doi:10.1073/pnas.91.2.529

Cited by 99 publications

(73 citation statements)

References 26 publications

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“…A positive effect of P (0.1-1 m) on forward (Contreras and Llanos, 2001) and hyperactivated (Uhler et al, 1992;Calogero et al, 1996;Jaiswal et al, 1999) motility has been reported by some authors but not confirmed by others (Kay et al, 1994;Wang et al, 2001;Luconi et al, 2004). The effect of P on hyperactivated motility was found to be transient and was not counteracted by P antagonists (Uhler et al, 1992;Yang et al, 1994). Recently, it has been found that P induces Ca 2+ oscillations, due to a release from intracellular stores (see also next) in the proximity of the flagellum, which are strictly related to the flagellar activity (Harper et al, 2004;Bedu-Addo et al, 2007), suggesting that this mechanism, rather than the massive Ca 2+ entry stimulated by the steroid, is responsible for induction of hyperactivation.…”

Section: P-induced Sperm Motilitymentioning

confidence: 86%

Nongenomic activation of spermatozoa by steroid hormones: Facts and fictions

Baldi

Luconi

Muratori

et al. 2009

Molecular and Cellular Endocrinology

139

154

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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.

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Section: P-induced Sperm Motilitymentioning

confidence: 86%

Nongenomic activation of spermatozoa by steroid hormones: Facts and fictions

Baldi

Luconi

Muratori

et al. 2009

Molecular and Cellular Endocrinology

139

154

View full text Add to dashboard Cite

show abstract

“…Therefore, we performed an inhibitor study using the potent antiprogestin, RU486. RU486 inhibits calcium uptake in sperm and counteracts the stimulation that is produced by progesterone (Yang et al, 1994). The rationale for using the inhibitor of progesterone to determine whether or not the acrosome reaction is the result of a specific progesterone action was that antiprogestin reverses the progesterone effects by competing with the binding sites of progesterone, assuming that progesterone induces the acrosome reaction through its specific receptors in spermatozoa.…”

Section: Discussionmentioning

confidence: 99%

RU486 Suppresses Progesterone-induced Acrosome Reaction in Boar Spermatozoa

Jang¹,

Yi²

2002

BMB Reports

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The effects of progesterone on the acrosome reaction, as well as the effects of RU486 on the progesterone-induced acrosome reaction in capacitated boar spermatozoa, were investigated. Progesterone, a major steroid that is secreted by the cumulus cells of oocyte, clearly induced the acrosome reaction in a dose-dependent manner in capacitated boar spermatozoa, even though it failed to show similar effects in non-capacitated spermatozoa. RU486, a potent antiprogestin, significantly reduced the effects of progesterone on the progesterone-induced acrosome reaction; however, when treated alone, it showed no inhibitory effects on the acrosome reaction. The inhibitory effects of RU486 were also shown to be dosedependent. These results imply that in addition to the wellknown inducer of the acrosome reaction, zona pellucida, progesterone can also induce the acrosome reaction through its specific receptors on spermatozoa after the spermatozoa undergo capacitation.

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“…Phospholipase C (PLC; Fukami et al 2003) and/or protein kinase A (Harrison et al 2000) are involved in progesteroneinduced AR. Progesterone also changes motility parameters (Yang et al 1994) and enhances hyperactivation in human (Sueldo et al 1993) and hamster spermatozoa (Noguchi et al 2008). Although progesterone enhances hyperactivation of human and hamster spermatozoa (Sueldo et al 1993, Noguchi et al 2008, the effective concentration of progesterone is different between humans and hamsters.…”

Section: Introductionmentioning

confidence: 99%

Suppression of progesterone-enhanced hyperactivation in hamster spermatozoa by estrogen

Fujinoki¹

2010

Reproduction

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In this study, I examined whether sperm hyperactivation in hamster is regulated by steroid hormones such as estrogen (estradiol, E 2 ) and progesterone. Although sperm hyperactivation was enhanced by progesterone, 17b-estradiol (17bE 2 ) itself did not affect sperm hyperactivation. However, 17bE 2 suppressed progesterone-enhanced hyperactivation in a concentration-dependent manner through non-genomic pathways when spermatozoa were exposed to 17bE 2 at the same time or before exposure to progesterone. When spermatozoa were exposed to 17bE 2 after exposure to progesterone, 17bE 2 did not suppress progesterone-enhanced hyperactivation. Moreover, 17a-estradiol, an inactive isomer of E 2 , did not suppress progesterone-enhanced hyperactivation. Observations using a FITC-conjugated 17bE 2 showed that it binds to the acrosome region of the sperm head. Binding of 17bE 2 to spermatozoa was not inhibited by progesterone, although 17bE 2 did not suppress progesterone-enhanced hyperactivation when spermatozoa were exposed to 17bE 2 after exposure to progesterone. On the other hand, binding of progesterone to spermatozoa was also not inhibited by 17bE 2 even if progesterone-enhanced hyperactivation was suppressed by 17bE 2 . Although tyrosine phosphorylations of sperm proteins were enhanced by progesterone, enhancement of tyrosine phosphorylations by progesterone was suppressed by 17bE 2 . Moreover, tyrosine phosphorylations were inhibited by 17bE 2 when only 17bE 2 was added to the medium. From these results, it is likely that 17bE 2 competitively suppresses progesterone-enhanced hyperactivation through the inhibition of tyrosine phosphorylations via non-genomic pathways.

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Progesterone and RU486: opposing effects on human sperm.

Cited by 99 publications

References 26 publications

Nongenomic activation of spermatozoa by steroid hormones: Facts and fictions

Nongenomic activation of spermatozoa by steroid hormones: Facts and fictions

RU486 Suppresses Progesterone-induced Acrosome Reaction in Boar Spermatozoa

Suppression of progesterone-enhanced hyperactivation in hamster spermatozoa by estrogen

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