Is there a role for the endocannabinoid system in the modulation of sperm capacitation within the female reproductive tract?

2008 ◽  
Vol 90 ◽  
pp. S323-S324 ◽  
Author(s):  
R. Talevi ◽  
L. Ricchiari ◽  
V. Barbato ◽  
A. Samo ◽  
S. De Lorio ◽  
...  
Keyword(s):  
Reproductive Tract ◽  
Endocannabinoid System ◽  
Female Reproductive Tract ◽  
Sperm Capacitation

scholarly journals Seminal vesicle proteins SVS3 and SVS4 facilitate SVS2 effect on sperm capacitation

Reproduction ◽  
2016 ◽  
Vol 152 (4) ◽  
pp. 313-321 ◽  
Author(s):  
Naoya Araki ◽  
Natsuko Kawano ◽  
Woojin Kang ◽  
Kenji Miyado ◽  
Kaoru Yoshida ◽  
...  
Keyword(s):  
Seminal Vesicle ◽  
Reproductive Tract ◽  
Female Reproductive Tract ◽  
The Other ◽  
Sperm Capacitation ◽  
Other Hand ◽  
Sperm Membrane ◽  
Vesicle Secretion ◽  
Mammalian Spermatozoa

Mammalian spermatozoa acquire their fertilizing ability in the female reproductive tract (sperm capacitation). On the other hand, seminal vesicle secretion, which is a major component of seminal plasma, inhibits the initiation of sperm capacitation (capacitation inhibition) and reduces the fertility of the capacitated spermatozoa (decapacitation). There are seven major proteins involved in murine seminal vesicle secretion (SVS1-7), and we have previously shown that SVS2 acts as both a capacitation inhibitor and a decapacitation factor, and is indispensable forin vivofertilization. However, the effects of SVSs other than SVS2 on the sperm have not been elucidated. Since mouseSvs2–Svs6genes evolved by gene duplication belong to the same gene family, it is possible that SVSs other than SVS2 also have some effects on sperm capacitation. In this study, we examined the effects of SVS3 and SVS4 on sperm capacitation. Our results showed that both SVS3 and SVS4 are able to bind to spermatozoa, but SVS3 alone showed no effects on sperm capacitation. On the other hand, SVS4 acted as a capacitation inhibitor, although it did not show decapacitation abilities. Interestingly, SVS3 showed an affinity for SVS2 and it facilitated the effects of SVS2. Interaction of SVS2 and spermatozoa is mediated by the ganglioside GM1 in the sperm membrane; however, both SVS3 and SVS4 had weaker affinities for GM1 than SVS2. Therefore, we suggest that separate processes may cause capacitation inhibition and decapacitation, and SVS3 and SVS4 act on sperm capacitation cooperatively with SVS2.

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

Reproduction ◽  
2013 ◽  
Vol 145 (3) ◽  
pp. 255-263 ◽  
Author(s):  
Lukas Ded ◽  
Natasa Sebkova ◽  
Martina Cerna ◽  
Fatima Elzeinova ◽  
Pavla Dostalova ◽  
...  
Keyword(s):  
Reproductive Tract ◽  
Negative Impact ◽  
Reproductive Potential ◽  
Female Reproductive Tract ◽  
Sperm Capacitation ◽  
Epididymal Sperm ◽  
Knock Out ◽  
17Β Estradiol

Estrogens play a crucial role in spermatogenesis and estrogen receptor α knock-out male mice are infertile. It has been demonstrated that estrogens significantly increase the speed of capacitation in vitro; however this may lead to the reduction of reproductive potential due to the decreased ability of these sperm to undergo the acrosome reaction. To date the in vivo effect of estrogens on the ability of sperm to capacitate has not been investigated. Therefore, in this study, we exposed mice (n=24) to 17β-estradiol (E2) at the concentration of 20 ng/ml either during puberty from the fourth to seventh week of age (n=8), or continuously from birth for a period of 12 weeks (n=8) at which age the animals from both groups were killed. The capacitation status of epididymal and testicular sperm was analysed by tyrosine phosphorylation (TyrP) antibody (immunofluorescence and western blot) and chlortetracycline (CTC) assay. According to our results, in vivo exposure to increased E2 concentrations caused premature sperm capacitation in the epididymis. The effect of E2, however, seems reversible because after the termination of the exposure premature epididymal sperm capacitation is decreased in animals treated during puberty. Furthermore the changes in epididymal sperm capacitation status detected by TyrP and CTC positively correlate with plasma levels of E2 and the expression of the estrogen-dependent trefoil factor 1 (Tff1) gene in testicular tissue. Therefore, our data implicate that in vivo exposure to E2 under specific conditions leads to the premature capacitation of mouse sperm in epididymis with a potential negative impact on the sperm reproductive fitness in the female reproductive tract.

Sperm capacitation in the human female reproductive tract**Supported by the National Institutes of Health grants HD-15149 and HD-03402.

1985 ◽  
Vol 43 (2) ◽  
pp. 325-327 ◽  
Author(s):  
Hovey Lambert ◽  
James W. Overstreet ◽  
Patricio Morales ◽  
Frederick W. Hanson ◽  
Ryuzo Yanagimachi
Keyword(s):  
Reproductive Tract ◽  
Female Reproductive Tract ◽  
National Institutes Of Health ◽  
Sperm Capacitation ◽  
Human Female

scholarly journals Effects of lactoferrin, a protein present in the female reproductive tract, on parameters of human sperm capacitation and gamete interaction

Andrology ◽  
2015 ◽  
Vol 3 (6) ◽  
pp. 1068-1075 ◽  
Author(s):  
C. M. Zumoffen ◽  
E. Massa ◽  
A. M. Caille ◽  
M. J. Munuce ◽  
S. A. Ghersevich
Keyword(s):  
Reproductive Tract ◽  
Human Sperm ◽  
Female Reproductive Tract ◽  
Sperm Capacitation ◽  
Gamete Interaction

scholarly journals Role of spermine in mammalian sperm capacitation and acrosome reaction

1991 ◽  
Vol 278 (1) ◽  
pp. 25-28 ◽  
Author(s):  
S Rubinstein ◽  
H Breitbart
Keyword(s):  
Binding Sites ◽  
Acrosome Reaction ◽  
Reproductive Tract ◽  
Female Reproductive Tract ◽  
Sperm Capacitation ◽  
Amino Groups ◽  
Binding Properties ◽  
Mammalian Sperm ◽  
Energy Dependent

The binding properties of seminal polyamines to ram spermatozoa and their possible role in sperm capacitation and the acrosome reaction were studied. Binding and release of [14C]spermine from ram spermatozoa occurred at a rate faster than in somatic cells and were not energy-dependent. Release of bound spermine was further facilitated by heparin, a constituent of the female reproductive tract which was reported to induce capacitation and the acrosome reaction. High- and low-affinity polyamine-binding sites were identified, of which the high-affinity site was specific to polyamines with three or more amino groups. We also found that spermine inhibited the acrosome reaction and propose that it is the major seminal decapacitating factor. Since precise timing of capacitation and the acrosome reaction are critical for successful fertilization, it is suggested that the role of seminal spermine is to prevent premature capacitation and the acrosome reaction.

The endocannabinoid system expression in the female reproductive tract is modulated by estrogen

2017 ◽  
Vol 174 ◽  
pp. 40-47 ◽  
Author(s):  
J. Maia ◽  
M. Almada ◽  
A. Silva ◽  
G. Correia-da-Silva ◽  
N. Teixeira ◽  
...  
Keyword(s):  
Reproductive Tract ◽  
Endocannabinoid System ◽  
Female Reproductive Tract

scholarly journals GIV/Girdin, a Non-receptor Modulator for Gαi/s, Regulates Spatiotemporal Signaling during Sperm Capacitation and is Required for Male Fertility

2021 ◽  
Author(s):  
Sequoyah Reynoso ◽  
Vanessa Castillo ◽  
Gajanan Dattatray Katkar ◽  
Inmaculada Lopez-Sanchez ◽  
Sahar Taheri ◽  
...  
Keyword(s):  
Male Fertility ◽  
Reproductive Tract ◽  
Cell Penetrating Peptides ◽  
Female Reproductive Tract ◽  
Signaling Cascades ◽  
Nucleotide Exchange ◽  
Sperm Capacitation ◽  
Receptor Modulator ◽  
Guanine Nucleotide Exchange ◽  
Shed Light

For a sperm to successfully fertilize an egg, it must first undergo capacitation in the female reproductive tract, and later undergo acrosomal reaction (AR) upon encountering an egg surrounded by its vestment. How premature AR is avoided despite rapid surges in signaling cascades during capacitation remains unknown. Using a combination of KO mice and cell-penetrating peptides, we show that GIV (CCDC88A), a guanine nucleotide-exchange modulator (GEM) for trimeric GTPases, is highly expressed in spermatocytes and is required for male fertility. GIV is rapidly phosphoregulated on key tyrosine and serine residues in human and murine spermatozoa. These phosphomodifications enable GIV-GEM to orchestrate two distinct compartmentalized signaling programs in the sperm tail and head; in the tail, GIV enhances PI3K→Akt signals, sperm motility and survival, whereas in the head it inhibits cAMP surge and premature AR. Furthermore, GIV transcripts are downregulated in the testis and semen of infertile men. These findings exemplify the spatiotemporally segregated signaling programs that support sperm capacitation and shed light on a hitherto unforeseen cause of infertility in men.

scholarly journals Expression of cystatin C in the female reproductive tract and its effect on human sperm capacitation

2018 ◽  
Vol 16 (1) ◽  
Author(s):  
Robert Kuo-Kuang Lee ◽  
Huan-Chin Tseng ◽  
Yuh-Ming Hwu ◽  
Chi-Chen Fan ◽  
Ming-Huei Lin ◽  
...  
Keyword(s):  
Cystatin C ◽  
Reproductive Tract ◽  
Human Sperm ◽  
Female Reproductive Tract ◽  
Sperm Capacitation

scholarly journals GIV/Girdin, a non-receptor modulator for Gαi/s, regulates spatiotemporal signaling during sperm capacitation and is required for male fertility

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Sequoyah Reynoso ◽  
Vanessa Castillo ◽  
Gajanan Dattatray Katkar ◽  
Inmaculada Lopez-Sanchez ◽  
Sahar Taheri ◽  
...  
Keyword(s):  
Male Fertility ◽  
Reproductive Tract ◽  
Cell Penetrating Peptides ◽  
Female Reproductive Tract ◽  
Conditional Knockout ◽  
Signaling Cascades ◽  
Nucleotide Exchange ◽  
Sperm Capacitation ◽  
Receptor Modulator ◽  
Guanine Nucleotide Exchange

For a sperm to successfully fertilize an egg, it must first undergo capacitation in the female reproductive tract and later undergo acrosomal reaction (AR) upon encountering an egg surrounded by its vestment. How premature AR is avoided despite rapid surges in signaling cascades during capacitation remains unknown. Using a combination of conditional knockout (cKO) mice and cell-penetrating peptides, we show that GIV (CCDC88A), a guanine nucleotide-exchange modulator (GEM) for trimeric GTPases, is highly expressed in spermatocytes and is required for male fertility. GIV is rapidly phosphoregulated on key tyrosine and serine residues in human and murine spermatozoa. These phosphomodifications enable GIV-GEM to orchestrate two distinct compartmentalized signaling programs in the sperm tail and head; in the tail, GIV enhances PI3K→Akt signals, sperm motility and survival, whereas in the head it inhibits cAMP surge and premature AR. Furthermore, GIV transcripts are downregulated in the testis and semen of infertile men. These findings exemplify the spatiotemporally segregated signaling programs that support sperm capacitation and shed light on a hitherto unforeseen cause of infertility in men.

Effect of Contraceptive Steroids on the Endometrium of Guinea Pig: SEM study

1977 ◽  
Vol 35 ◽  
pp. 668-669
Author(s):  
Mai M. Said ◽  
Ramesh K. Nayak ◽  
Randall E. McCoy
Keyword(s):  
Guinea Pig ◽  
Reproductive Tract ◽  
Three Dimensional ◽  
Female Reproductive Tract ◽  
Human Female ◽  
Surface Ultrastructure ◽  
Transmission Electron ◽  
Sem Study ◽  
Uterine Mucosa ◽  
Group 1

Burgos and Wislocki described changes in the mucosa of the guinea pig uterus, cervix and vagina during the estrous cycle investigated by transmission electron microscopy. More recently, Moghissi and Reame reported the effects of progestational agents on the human female reproductive tract. They found drooping and shortening of cilia in norgestrel and norethindrone- treated endometria. To the best of our knowledge, no studies concerning the effects of mestranol and norethindrone given concurrently on the three-dimensional surface features on the uterine mucosa of the guinea pig have been reported. The purpose of this study was to determine the effect of mestranol and norethindrone on surface ultrastructure of guinea pig uterus by SEM.Seventy eight animals were used in this study. They were allocated into two groups. Group 1 (20 animals) was injected intramuscularly 0.1 ml vegetable oil and served as controls.

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