Effects of Alcohol on Polyphosphoinositide‐Mediated Intracellular Signaling<sup>a</sup>

Hoek, Jan B.; Higashi, Katsuyoshi

doi:10.1111/j.1749-6632.1991.tb33865.x

Cited by 13 publications

(8 citation statements)

References 16 publications

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“…Embryos treated with 100 IM OAG compacted within 20 min and remained compacted as long as the synthetic diacylglycerol was present (data not shown). Although 10 ng/ml PMA induced compaction within 20 min, it also caused the embryos to fully decompact after 40 min and maintained them in a decompacted state as long as it was present, presumably due to its ability to down-regulate PKC [29,37,39]. Embryos pretreated with 30 AIM sphingosine or 500 nM calphostin C, two PKC-specific inhibitors, failed to compact after exposure to PMA, indicating that PKC activity required for compaction was inhibited at these concentrations of sphingosine and calphostin C.…”

Section: Resultsmentioning

confidence: 96%

Regulation of Blastocoele Formation by Intracellular Calcium Release is Mediated through a Phospholipase C-Dependent Pathway in Mice1

Stachecki¹,

Armant²

1996

Biology of Reproduction

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Calcium signaling plays a critical role in the regulation of mouse preimplantation development, in part through the activation of calmodulin. Calcium transients in mouse morulae appear to be generated predominantly through the production of inositol 1,4,5-trisphosphate (IP3) by phospholipase C (PLC). IP3 receptors predominate in mouse embryos as regulators of calcium release. Exposure to the PLC inhibitors ET-18-OCH3 or U73122 resulted in a dose-dependent, reversible inhibition of cavitation, while the inactive analogue U73343 did not alter the rate of cavitation, as compared to that in controls. U73122 inhibited the release of calcium from intracellular stores after exposure to ethanol or lysophosphatidic acid, suggesting that PLC is required for blastocoele formation in the mouse and that calcium signaling may be PLC-dependent. In addition to IP3, PLC activation generates diacylglycerol, which stimulates protein kinase C (PKC) and could also alter the rate of embryonic development. However, activation of PKC with phorbol ester or synthetic diacylglycerol was not sufficient to accelerate development, although embryo culture in medium containing PKC inhibitors did delay cavitation. Exposure to a PKC inhibitor during ethanol-induced calcium signaling did not attenuate the ensuing acceleration of cavitation. These results demonstrate that a PLC-mediated signaling pathway is required for blastocoele formation and that the generation of IP3, but not diacylglycerol, is critical for accelerating preimplantation development.

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Section: Resultsmentioning

confidence: 96%

Regulation of Blastocoele Formation by Intracellular Calcium Release is Mediated through a Phospholipase C-Dependent Pathway in Mice1

Stachecki¹,

Armant²

1996

Biology of Reproduction

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“…We concluded this from results in nonpancreatic cells showing that ethanol influences PKC subcellular distribution and activity [21][22][23][24][25] and that it induces transformations of the actin cytoskeleton [26][27][28]. However, to our knowledge, pancreatic acinar cells have not yet been tested for such effects of ethanol.…”

Section: Introductionmentioning

confidence: 81%

Ethanol modifies the actin cytoskeleton in rat pancreatic acinar cells — Comparison with effects of CCK

et al. 2004

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“…Although the mechanism of ethanol as an effector molecule is not clear, it has been suggested in different cell models that ethanol could modify plasma membrane fluidity by changing proteinprotein interactions and, in consequence, activating proteins such as PLC with the production of IP 3 Hoek and Higashi, 1991). In addition, ethanol generates increases of intracellular Ca 2+ levels , activates PKC (Gordon et al, 2001) and modifies the cytoskeleton's actin distribution (Rubin and Hoek, 1988).…”

Section: Discussionmentioning

confidence: 99%

“…In other cell models ethanol treatment induced activation of phospholipase C (PLC), generation of inositol-3-phosphate (IP 3), increase of cytoplasmic Ca 2+ and activation of protein kinase C (PKC) (Hoek et al, 1987;Hoek and Higashi, 1991;Gordon et al, 2001;Zhang et al, 2001). On view of the ethanol effects on Ca 2+ regulation and microneme secretion, and the role of Ca 2+ in conoid extrusion, we investigated whether ethanol could be an adequate inducer for conoid extrusion in isolated T. gondii tachyzoites.…”

Section: Introductionmentioning

confidence: 99%

Induction and regulation of conoid extrusion inToxoplasma gondii

Carmen

Mondragón

González

et al. 2009

Cellular Microbiology

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SummaryCell invasion by the intracellular parasite Toxoplasma gondii occurs through an active process that involves dynamic events, such as gliding motility and conoid extrusion, followed by a sequential secretion from specialized secretory organelles. Increase of intracellular Ca2+ by ionophores induces conoid extrusion, although in an irreversible way, thus limiting the characterization of the regulatory pathways. In this report we studied the effect of different activating conoid conditions to characterize the regulatory mechanisms involved. Exposure of tachyzoites to ethanol, a well-known activator of microneme secretion through the increase of intracellular Ca 2+, induced conoid extrusion without affecting parasite viability nor its in vitro invasive capability, in a process that could be completely reverted and repeatedly reactivated. A temporal relationship between conoid extrusion and microneme secretion was here studied. Under this condition, signal transduction pathways and the precise role of the parasite cytoskeleton were characterized. Our results indicate that phospholipase C, Ca 2+ released through channels sensitive to inositol-3-phosphate and ryanodine, as well as myosin together with actin filaments, but not microtubules, all participate in conoid extrusion. Specific inhibitors for serine-threonine kinases blocked conoid extrusion; in contrast, calmodulin inhibitors did not affect the induction. A regulatory model for conoid activation is here proposed.

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Effects of Alcohol on Polyphosphoinositide‐Mediated Intracellular Signaling^a

Cited by 13 publications

References 16 publications

Regulation of Blastocoele Formation by Intracellular Calcium Release is Mediated through a Phospholipase C-Dependent Pathway in Mice1

Regulation of Blastocoele Formation by Intracellular Calcium Release is Mediated through a Phospholipase C-Dependent Pathway in Mice1

Ethanol modifies the actin cytoskeleton in rat pancreatic acinar cells — Comparison with effects of CCK

Induction and regulation of conoid extrusion inToxoplasma gondii

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Effects of Alcohol on Polyphosphoinositide‐Mediated Intracellular Signalinga

Cited by 13 publications

References 16 publications

Regulation of Blastocoele Formation by Intracellular Calcium Release is Mediated through a Phospholipase C-Dependent Pathway in Mice1

Regulation of Blastocoele Formation by Intracellular Calcium Release is Mediated through a Phospholipase C-Dependent Pathway in Mice1

Ethanol modifies the actin cytoskeleton in rat pancreatic acinar cells — Comparison with effects of CCK

Induction and regulation of conoid extrusion inToxoplasma gondii

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Effects of Alcohol on Polyphosphoinositide‐Mediated Intracellular Signaling^a