Molecular physiology and pathology of Ca2+-conducting channels in the plasma membrane of mammalian sperm

Felix, Ricardo

doi:10.1530/rep.1.00478

Cited by 47 publications

(47 citation statements)

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“…These changes must be achieved by modifications of existing proteins, rather than changes in gene expression, and are modulated by signals from the sperm's environment or may occur spontaneously. As in many mammals, sperm capacitation in pigs requires Ca 2+ and bicarbonate [7,8]: the sequence of events for pig sperm capacitation is similar to that of other species. In particular, tyrosine phosphorylation of mouse, human, bull and hamster sperm proteins is closely associated with capacitation [9][10][11].…”

mentioning

confidence: 75%

Cytochrome c Upregulation during Capacitation and Spontaneous Acrosome Reaction Determines the Fate of Pig Sperm Cells: Linking Proteome Analysis

Choi

Uhm

Song

et al. 2008

Journal of Reproduction and Development

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Abstract.To identify the mechanisms underlying capacitation, we undertook a high-resolution differential proteomic analysis of pig sperm cells. Two-dimensional gel electrophoresis and subsequent MALDI-TOF mass spectrometry analyses led to identification of 56 differentially expressed proteins. After induction of capacitation in vitro, the wellestablished markers of the capacitation (lactadherin P47, acrosomal protein SP-10 precursor, prohibitin, proteasomes, DJ-1 protein and arylsulfatase-A) and TCA cycle proteins (isocitrate dehydrogenase, malate dehydrogenase and pyruvate dehydrogenase) were identified. During induction, cytochrome c expression via the p53 pathway increased, however apoptotic executors, such as caspase-3, decreased significantly. Therefore, we tested the hypothesis that cytochrome c upregulation in spermatozoa is capable of activating tyrosine phosphorylation for capacitation, rather than apoptosis. Exposure of sperm cells to soluble Na2CrO4 [Cr (VI)], which induces cytochrome c upregulation, caused a dose-and time-dependent increase in tyrosine phosphorylation of sperm proteins in non-capacitating medium. In contrast, supplementation of cyclosporin A, which blocks cytochrome c upregulation, inhibited tyrosine phosphorylation of sperm proteins. Furthermore, spermatozoa in capacitation medium or non-capacitation media supplemented with soluble Cr (VI) showed similar levels of capacitation. These findings indicate that differential expression of many of these proteins has previously been unrecognized in sperm cells incubated in capacitation medium also suggest that a gradual increase of cytochrome c during incubation to induce capacitation determines sperm cell fate, i.e., apoptosis or further development for fertilization. Key words: Capacitation, Cytochrome c upregulation, 2-dimensional gel electrophoresis, Pig, Sperm maturation (J. Reprod. Dev. 54: [68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83] 2008) permatozoa are terminally differentiated and specialized cells [1]. The deficiencies of major transcriptional and translational activities of sperm are generally known [2] however, recent published evidence shows that sperm are capable of producing major nuclear gene expressions using 55S mitochondrial ribosomes during their residence in the female reproductive tract until fertilization [3]. Mature sperm cells are released from the testis with tightly supercoiled, transcriptionally inert DNA [4]. In addition, they do not exhibit progressive motility, but acquire this ability during passage through the epididymis. These processes are referred to as maturation; other maturational changes include completion of nuclear condensation and changes in the expression and distribution of molecules on the cell surface [1]. Therefore, freshly ejaculated sperm cells are incapable of fertilization and must spend some time in a suitable environment in order to capacitate.Capacitation in all mammals involves shedding of the sperm plasma membrane followed by hyperactivity of the tail, attachme...

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mentioning

confidence: 75%

Cytochrome c Upregulation during Capacitation and Spontaneous Acrosome Reaction Determines the Fate of Pig Sperm Cells: Linking Proteome Analysis

Choi

Uhm

Song

et al. 2008

Journal of Reproduction and Development

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“…However, studies of Ca 2+ -regulation in sperm suggest that the 'standard' components and Ca 2+ -signaling capabilities are retained, though possibly in modified form (Wennemuth et al, 2003;Publicover et al, 2007). Immunohistochemistry and Western blotting experiments show that several types of VOCCs are present (Felix, 2005;Jagannathan et al, 2006) and there is also good evidence for expression of ligand-activated channels (Meizel, 2004) and cyclic nucleotide-regulated channels (Weyand et al, 1994;Gauss et al, 1998;Galindo et al, 2000;Kobori et al, 2000) in mammalian and invertebrate sperm, In addition, a number of studies have shown that capacitative Ca 2+ influx occurs in sperm (Blackmore, 1993;1999;Dragileva et al, 1999;O'Toole et al, 2000;Rossato et al, 2001), indicating that store-operated channels are also present. Ca 2+ -ATPase extrusion pumps in the plasma membrane are probably the greatest contributors to Ca 2+ buffering in mammalian sperm (Wennemuth et al, 2003) and are potentially involved in regulating [Ca 2+ ] changes during capacitation (Fraser and McDermott, 1992;DasGupta et al, 1994).…”

Section: Cellular [Ca 2+ ] Regulationmentioning

confidence: 99%

“…Though understanding of the physiology of male germ cells is (arguably) some way behind that for somatic cells, it is well established that changes in Ca 2+ -signalling regulate or contribute to the regulation of many aspects of mammalian sperm function (Darszon et al, 2005;Felix, 2005;Jimenez-Gonzalez et al, 2006;Zhang et al, 2006;Publicover et al, 2007). [Ca 2+ ] i has been shown to increase during capacitation in several mammalian species (Yanagimachi, 1994) including human (Baldi et al, 1991;Garcia and Meizel, 1999) and has both negative and positive actions on capacitation and related signalling events (Visconti et al, 2002).…”

mentioning

confidence: 99%

Mobilisation of stored calcium in the neck region of human sperm a mechanism for regulation of flagellar activity

Bedu-Addo¹,

Costello²,

Harper³

et al. 2008

Int. J. Dev. Biol.

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Calcium signalling plays a pivotal role in sperm physiology, being intimately involved in the regulation of acrosome reaction, chemotaxis and hyperactivation. Here we describe briefly the mechanisms of calcium regulation in somatic cells and the ways in which these mechanisms have been adapted to function in mature spermatozoa. We then consider recent data from this and other laboratories on the responses of sperm to three compounds: progesterone and nitric oxide (both products of the cumulus oophorus) and 4-aminopyridine. All of these compounds induce calcium signals in the posterior sperm head and neck region and, when applied at appropriate concentrations, modify flagellar activity, causing asymmetric bending of the proximal flagellum. We argue that these effects reflect a common mode of action, mobilisation of calcium stored in the sperm neck region. Finally we consider the nature of calcium signalling pathways in sperm. We suggest that this highly specialised and extremely polarised cell, though working with the same calcium signalling 'tools' as those of somatic cells, employs them to generate unusually 'hard-wired' calcium signals that do not act to integrate stimuli. 'Leakage' between these calcium signalling pathways will generate inappropriate responses, compromising functioning of the cell.

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“…These include primary ciliary dyskinesia (Kartagener syndrome), dysplasia of the fibrous sheath of the sperm flagellum, retinitis pigmentosa, and Usher syndrome (review: 32). More recently, mutations in two calcium-permeable ion channels, CatSper2 and polycystin-2, have been linked to the production of asthenozoospermia (review: 35,43). Although studies on these conditions have produced interesting genetic and molecular information, the etiology for the majority of cases with poor motility remains unknown.…”

Section: Discussionmentioning

confidence: 99%

“…Normal sperm motility is primarily controlled by cAMP/PKA and calcium signaling pathways which probably interact by controlling, respectively, phosphorylation and dephosphorylation of proteins in the sperm tail (32)(33)(34)(35)(36). The calcium signaling pathway involves calcium influx through ion channels on the sperm tail plasma membrane, activation of calmodulin and calcium/calmodulin-dependent serine/threonine protein kinase IV (CaMK IV; 37), activation of additional calcium channels and finally activation of calcineurin, a calcium/calmodulin-dependent serine/threonine phosphatase.…”

Section: Introductionmentioning

confidence: 99%

Link between low-dose environmentally relevant cadmium exposures and asthenozoospermia in a rat model

Benoff

Auborn

Marmar

et al. 2008

Fertility and Sterility

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Objective-To define the mechanism(s) underlying an association between asthenozoospermia and elevated blood, seminal plasma and testicular cadmium levels in infertile human males using a rat model of environmentally relevant cadmium exposures.Setting-University medical center andrology research laboratory. Animals-MaleWistar rats (n = 60), documented to be sensitive to the testicular effects of cadmium.Interventions-Rats were given ad libitum access to water supplemented with 14% sucrose and 0, 5, 50 or 100 mg/L cadmium for 1, 4 or 8 weeks being at puberty.Main outcome measure(s)-Testicular cadmium levels were determined by atomic absorption, cauda epididymal sperm motility by visual inspection, and testicular gene expression by DNA microarray hybridization.Results-Chronic, low dose cadmium exposures produced a time-and dose-dependent reduction in sperm motility. Transcription of genes regulated by calcium and expression of L-type voltagedependent calcium channel mRNA splicing variants were altered by cadmium exposure. Expression of calcium binding proteins involved in modulation of sperm motility was unaffected. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Presented at the UCSF-CHE Summit on Environmental Challenges to Reproductive Health and Fertility, UCSF Mission Bay Conference Center, San Francisco, California, January 28-30, 2007. NIH Public Access Conclusions-A causal relationship between elevated testicular cadmium and asthenozoospermia was identified. Aberrrant sperm motility was correlated with altered expression of L-type voltagedependent calcium channel isoforms found on the sperm tail, which regulate calcium and cadmium influx.

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Molecular physiology and pathology of Ca2+-conducting channels in the plasma membrane of mammalian sperm

Cited by 47 publications

References 103 publications

Cytochrome c Upregulation during Capacitation and Spontaneous Acrosome Reaction Determines the Fate of Pig Sperm Cells: Linking Proteome Analysis

Cytochrome c Upregulation during Capacitation and Spontaneous Acrosome Reaction Determines the Fate of Pig Sperm Cells: Linking Proteome Analysis

Mobilisation of stored calcium in the neck region of human sperm a mechanism for regulation of flagellar activity

Link between low-dose environmentally relevant cadmium exposures and asthenozoospermia in a rat model

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