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Lopes, Carlos H.G.L.; Mazzini, María N.; Tortorella, Helen; Konrath, Renato Augusto; Brandelli, Adriano

doi:10.1023/a:1006982919464

Cited by 15 publications

References 23 publications

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Suppression effect of seminal vesicle autoantigen on platelet‐activating factor‐induced mouse sperm capacitation

Huang

Chen

Lin

et al. 2006

J of Cellular Biochemistry

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Mammalian sperm gain the ability to fertilize an egg successfully by the capacitation process. An unregulated capacitation process causes sperm to undergo a spontaneous acrosome reaction (AR) and resulting in loss of their fertilization activity. Thus, functional sperm activation is tightly regulated by a capacitation and suppression (decapacitation) mechanism. Factors, such as platelet-activating factor (PAF) present in both sperm and the female genital tract, are able to stimulate sperm capacitation. Seminal plasma is thought to have the ability to suppress sperm capacitation; however, the regulatory mechanisms of seminal plasma protein on sperm capacitation are not well understood. Recently, we demonstrated that seminal vesicle autoantigen (SVA), a major seminal vesicle secretory protein, is able to suppress mouse sperm capacitation. To further study the suppression spectra of SVA on sperm capacitation, we investigated the effect of SVA on PAF-induced mouse sperm capacitation-related signals. Here, we demonstrate that SVA decreases the [Ca(2+)](i) to suppress the PAF's effects on [Ca(2+)](i), the cAMP level, protein tyrosine phosphorylation, and capacitation. The inhibition of PAF-induced protein tyrosine phosphorylation and capacitation by SVA can be reversed by cAMP agonists. Characterization of the interactions of SVA with PAF by TLC overlay and tryptophan fluorescence spectrum analyses indicates that SVA is capable of binding PAF with an apparent dissociation constant K(d) > 50 microM. Together with these results, we demonstrate that SVA deceases [Ca(2+)](i) and cross-talks with PAF-induced intracellular signals to regulate mouse sperm capacitation.

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Suppression effect of seminal vesicle autoantigen on platelet‐activating factor‐induced mouse sperm capacitation

Huang

Chen

Lin

et al. 2006

J of Cellular Biochemistry

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Capacitation suppression by mouse seminal vesicle autoantigen involves a decrease in plasma membrane Ca²⁺‐ATPase (PMCA)‐mediated intracellular calcium

Yen

Ling

et al. 2010

J of Cellular Biochemistry

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Successful fertilization is tightly regulated by capacitation and decapacitation processes. Without appropriate decapacitation regulation, sperm would undergo a spontaneous acrosome reaction which leads to loss of fertilization ability. Seminal plasma is known to negatively regulate sperm capacitation. However, the suppressive mechanisms still remain unclear. In this study, we demonstrate the decapacitation mechanism of mouse seminal vesicle autoantigen (SVA) might target membrane sphingomyelin (SPM) and regulate plasma membrane Ca(2+)-ATPase (PMCA) activity. The SVA was shown to suppress sperm capacitation induced by a broad panel of capacitation factors (bovine serum albumin (BSA), PAF, and cyclodextrin (CD)). Furthermore, SVA significantly decreased [Ca(2+)](i) and NaHCO(3)-induced [cAMP](i). Cyclic AMP agonists bypassed the SVA's suppressive ability. Importantly, the SVA may regulate PMCA activity which was evidenced by the fact that the SVA decreased the [Ca(2+)](i) and intracellular pH (pH(i)) of sperm; meanwhile, a PMCA inhibitor (carboxyeosin) could reverse SVA's suppression of [Ca(2+)](i). The potential target of the SVA on membrane SPM/lipid rafts was highlighted by the high binding affinity of SPM-SVA (with a K(d) of ~3 µM) which was close to the IC(50) of SVA's suppressive activity. Additionally, treatment of mink lung epithelial cells with the SVA enhanced plasminogen activator inhibitor (PAI)-1 expression stimulated by tumor growth factor (TGF)-β and CD. These observations supported the membrane lipid-raft targeting of SVA. In summary, in this paper, we demonstrate that the decapacitation mechanism of the SVA might target membrane sphingolipid SPM and regulate PMCA activity to lower [Ca(2+)](i), thereby decreasing the [cAMP](i) level and preventing sperm pre-capacitation.

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Effects of methyl‐β‐cyclodextrin‐mediated cholesterol depletion in porcine sperm compared to somatic cells

Gestel

Helms

Brouwers

et al. 2005

Molecular Reproduction Devel

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In this study, the use of methyl-beta-cyclodextrin (MBCD) to support capacitation of sperm cells was studied. Sperm were incubated with MBCD or alternatively capacitated in an in vitro fertilization medium. The effects of these incubations on phospholipid scrambling (using merocyanin), cholesterol depletion, GM-1 localization (using cholera-toxin B (CTX)), and membrane deterioration were assessed. For comparison, this was also tested in MBCD-treated MDCK cells. In MDCK cells, upto 71% of cholesterol was depleted, which coincided with a more diffuse CTX staining without any obvious effects on cell viability. In sperm, a similar depletion of 53% cholesterol was found after a 10 mM MBCD treatment. However, no merocyanin response was observed in viable sperm after MBCD treatments (indicating a lack of membrane changes associated with sperm capacitation). In contrast to MDCK, cells >1 mM MBCD caused plasma membrane disintegration and rendered sperm immotile. At higher concentrations also acrosome disruption was noted. CTX staining was absent at < 0.1 mM MBCD incubations but appeared at higher MBCD levels and was found to be specific for deteriorated cells that showed morphological signs of acrosome disruption. No significant plasma membrane deterioration, acrosome disruption, and sperm immotility nor CTX staining and only a modest (< 15%) cholesterol depletion were observed in conventionally capacitated sperm, where 40% of the intact sperm showed merocyanin staining. Taken together, the results indicate that membranes of sperm are more sensitive to MBCD-mediated cholesterol depletion than MDCK cells and that the use of MBCD to support sperm capacitation cannot be recommended due to its spermicidal effects.

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Cited by 15 publications

References 23 publications

Suppression effect of seminal vesicle autoantigen on platelet‐activating factor‐induced mouse sperm capacitation

Suppression effect of seminal vesicle autoantigen on platelet‐activating factor‐induced mouse sperm capacitation

Capacitation suppression by mouse seminal vesicle autoantigen involves a decrease in plasma membrane Ca²⁺‐ATPase (PMCA)‐mediated intracellular calcium

Effects of methyl‐β‐cyclodextrin‐mediated cholesterol depletion in porcine sperm compared to somatic cells

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Untitled

Cited by 15 publications

References 23 publications

Suppression effect of seminal vesicle autoantigen on platelet‐activating factor‐induced mouse sperm capacitation

Suppression effect of seminal vesicle autoantigen on platelet‐activating factor‐induced mouse sperm capacitation

Capacitation suppression by mouse seminal vesicle autoantigen involves a decrease in plasma membrane Ca2+‐ATPase (PMCA)‐mediated intracellular calcium

Effects of methyl‐β‐cyclodextrin‐mediated cholesterol depletion in porcine sperm compared to somatic cells

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Capacitation suppression by mouse seminal vesicle autoantigen involves a decrease in plasma membrane Ca²⁺‐ATPase (PMCA)‐mediated intracellular calcium