Development of in vitro fertilized mouse embryos exposed to ethanol during the preimplantation period: Accelerated embryogenesis at subtoxic levels

Leach, Richard E.; Stachecki, James J.; Armant, D. Randall

doi:10.1002/tera.1420470110

Cited by 52 publications

(47 citation statements)

References 19 publications

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“…Sr 2+ exposure during the first mitosis induces oscillations in parthenogenotes and resulting blastocysts have more cells in the inner cell mass (Bos-Mikich et al, 1995). Improved development has also been noted following exposure of oneor two-cell (but not four-cell) embryos to low concentrations of ethanol (Leach et al, 1993), a treatment that might increase [Ca 2+ ] i . A similar phenomenon has been described following fertilization, when Ca 2+ oscillation regimen can influence longterm developmental potential (Ozil and Huneau, 2001;Ducibella et al, 2002).…”

Section: Role Of Mitotic Ca 2+ Release In Mouse Embryosmentioning

confidence: 89%

An increase in [Ca2+]i is sufficient but not necessary for driving mitosis in early mouse embryos

FitzHarris

Larman

Richards

et al. 2005

Journal of Cell Science

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An increase in intracellular Ca2+ concentration ([Ca2+]i) has been shown to drive sea-urchin embryos and some fibroblasts through nuclear-envelope breakdown (NEBD) and the metaphase-to-anaphase transition. Mitotic Ca2+ transients can be pan-cellular global events or localized to the perinuclear region. It is not known whether Ca2+ is a universal regulator of mitosis or whether its role is confined to specific cell types. To test the hypothesis that Ca2+ is a universal regulator of mitosis, we have investigated the role of Ca2+ in mitosis in one-cell mouse embryos. Fertilized embryos generate Ca2+ transients during the first mitotic division. Imposing a Ca2+ transient by photorelease of inositol (1,4,5)-trisphosphate [Ins(1,4,5)P3] resulted in acceleration of mitosis entry, suggesting that a [Ca2+]i increase is capable of triggering mitosis. Mitotic Ca2+ transients were inhibited using three independent approaches: injection of intracellular Ca2+ buffers; downregulation of Ins(1,4,5)P3 receptors; and removal of extracellular Ca2+. None of the interventions had any effects on the timing of NEBD or cytokinesis. The possibility that NEBD is driven by localized perinuclear Ca2+ transients was examined using two-photon microscopy but no Ca2+-dependent increases in fluorescence were found to precede NEBD. Finally, the second mitotic division took place in the absence of any detectable [Ca2+]i increase. Thus, although an induced [Ca2+]i increase can accelerate mitosis entry, neither cytosolic nor perinuclear [Ca2+] increases appear to be necessary for progression through mitosis in mouse embryos.

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Section: Role Of Mitotic Ca 2+ Release In Mouse Embryosmentioning

confidence: 89%

An increase in [Ca2+]i is sufficient but not necessary for driving mitosis in early mouse embryos

FitzHarris

Larman

Richards

et al. 2005

Journal of Cell Science

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“…It is recognized that several events during early embryo develop induce defined calcium signaling events. For example: (1) calcium transients occur in the mouse zygote as a consequence of fertilization and these enhance the viability of embryos (Leach et al 1993, Stachecki et al 1994; (2) embryo-derived paf (1-o-alkyl-2-acetyl-snglycero-3-phosphocholine) caused periodic [Ca 2C ] i transients in the late zygote and mid-cycle two-cell stage, these transients are also necessary for normal survival of embryos in vitro (Emerson et al 2000, Lu et al 2004; (3) calcitonin-induced [Ca 2C ] i transients in four-cell to blastocyst stage embryos; and (4) lysophosphatidic acid-induced [Ca 2C ] i transients in blastocysts, which resulted in transient accumulation of heparinbinding EGF-like growth factor on the blastocyst surface (Liu & Armant 2004). This study offers the possibility that activation of Creb1 may be a mechanism of transducing these signaling events into altered patterns of Creb1-mediated transcription.…”

Section: Discussionmentioning

confidence: 99%

cAMP-responsive element-binding protein expression and regulation in the mouse preimplantation embryo

Jin¹,

O’Neill²

2007

Reproduction

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Gene expression from the new embryonic genome is required for normal preimplantation embryo development. Two members of the cAMP-responsive element-binding protein (Creb) family of transcription factors, Creb1 and activating transcription factor 1 (Atf1), are essential for normal preimplantation development. These transcription factors are activated by phosphorylation. Creb1 mRNA was expressed throughout the preimplantation phase. Cytoplasmic immunolocalization of Creb1 was detected in all preimplantation embryo stages. The antigen was largely excluded from the pronuclei/nuclei at embryonic stages except in the mid-cycle two-cell and compacted eight-cell embryo. Activation-state-specific antibodies showed serine 133 phosphorylated Creb1 localization was similar to Creb1 staining, except that there was no increase in staining at the eight-cell stage. Increased staining of phosphorylated Creb1 was observed in the nucleus of mid-cycle two-cell embryos. Increased expression of phosphorylated Creb1 in the two-cell embryo was induced by brief exposure of embryos to ionomycin, but not by a dibutyryl cAMP. This was blocked by buffering intracellular calcium with 1,2-bis(2-aminophenoxy)ethane-N,N,N 0 ,N 0 -tetraacetic acid tetrakis (acetoxymethyl ester), but not by a cAMP antagonist, Rp-cyclic 3 0 ,5 0 -hydrogen phosphorothioate adenosine. Calmodulin is an intracellular receptor for calcium. Calmodulin mRNA was expressed throughout the preimplantation phase of development. The calmodulin antagonist, W-7, inhibited the ionomycin-induced localization of phosphorylated Creb1 in the nucleus. Treatment of embryos with W-7 caused a dose-dependent inhibition of normal development of zygotes to the blastocysts stage. The study shows Creb1 expression and nuclear localization was dynamically regulated in the early embryo. The marked nuclear accumulation and phosphorylation of Creb1 at the two-cell stage occurred at the time of transcription from the embryonic genome and was regulated in a calcium-and calmodulin-dependent manner.

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“…Blastocysts previously exposed to 0.1% ethanol during the 1-cell stage appeared to form adhesive trophoblasts earlier than control embryos, indicating that ethanol exposure can induce precocious differentiation of the trophoblast cells. The ethanol treated blastocysts contained significantly more cells than control blastocysts [47]. These results indicate that ethanol can alter preimplantation development by both inhibiting or accelerating cell growth and differentiation [47].…”

Section: Discussionmentioning

confidence: 79%

“…The ethanol treated blastocysts contained significantly more cells than control blastocysts [47]. These results indicate that ethanol can alter preimplantation development by both inhibiting or accelerating cell growth and differentiation [47].…”

Section: Discussionmentioning

confidence: 79%

“…The similar result about blastocyst formation, in addition to different concentration of ethanol and exposure time is probably because of more sensitivity and vulnerability of developmental stages to higher concentrations and longer exposure of ethanol as a teratogen [46]. Leach et al [47] showed that one or two-cell embryos cultivated in a medium containing 1.6% ethanol had some problems for reaching to blastocyst stage. Ethanol exposure either arrested or enhanced normal development, depending on dose and embryonic stage of exposure.…”

Section: Discussionmentioning

confidence: 81%

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Can Ethanol Enhance the Cleavage and Development of Blocked Two-cell Embryos?

Darabi¹,

Shiravi²,

Azindokht³

2011

IJBBB

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Abstract-Arresting in a certain step of development, like two-cell stage could be one of the reasons of infertility. In this study, we evaluate the effects of ethanol on growth and development of mouse two-cell arrested embryos. In this xperimental study 4-6 week-old female mice were coupled with males following superovulation by intraperitoneal injection of pregnant mere serum gonadotropin (PMSG). Positive vaginal plug mice were killed 48 hours after human chorionic gonadotropin (hCG) injection. Two-cell embryos were transferred to culture medium, and divided in three groups, 1(control 1), 2 (control 2) and 3 (experimental). Second and third groups were exposed to 4º C for 24 hours in order to arrest the two-cell embryos. Group 2 were incubated immediately in 38º C, while group 3 were exposed to 0.1% ethanol for five minutes and group 1 were incubated without any exposure to low temperature. The developmental rate of embryos exposed to low temperature (4º C) were significantly decreased and retarded (P=0.001). There was no significant difference in the mean percent of cleavage rate between groups, but the mean percent of degenerated embryos (P=0.045), morula formation (P=0.005), blastocyst formation (P=0.014) and hatched blastocyst (P=0.001) in 120 h study, were significantly different between groups. The effect of 0.1% ethanol on arrested two-cell embryos can significantly enhance the mean percent of morula formation and development of blastocysts and hatching blastocysts comparing to 2 nd control group, without any significant effect on cleavage rate.

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Development of in vitro fertilized mouse embryos exposed to ethanol during the preimplantation period: Accelerated embryogenesis at subtoxic levels

Cited by 52 publications

References 19 publications

An increase in [Ca2+]i is sufficient but not necessary for driving mitosis in early mouse embryos

An increase in [Ca2+]i is sufficient but not necessary for driving mitosis in early mouse embryos

cAMP-responsive element-binding protein expression and regulation in the mouse preimplantation embryo

Can Ethanol Enhance the Cleavage and Development of Blocked Two-cell Embryos?

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