Blastocyst Cavitation is Accelerated by Ethanol- or Ionophore-Induced Elevation of Intracellular Calcium1

Stachecki, James J.; Yelian, Frank D.; Schultz, J F; Leach, Richard E.; Armant, D. Randall

doi:10.1095/biolreprod50.1.1

Cited by 54 publications

(44 citation statements)

References 54 publications

(72 reference statements)

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“…The post-fertilization calcium oscillations and the transients associated with nuclear envelope breakdown require factor(s) derived from the sperm that become associated with the nuclear membrane. There is no direct evidence of a developmental requirement for calcium transients in the mammalian early embryo outside these defined periods, although evidence that induction of artificial transients in morulae enhanced the rate of blastocyst formation (18,19) and the inhibition of embryo development by a calmodulin antagonist (W-7) suggests a role (20). It was recently shown (21) that exogenous PAF may induce calcium transients in the 2-cell mouse embryo although a mechanism for this action was not defined, nor was it established whether embryo-derived PAF also induced such responses.…”

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confidence: 99%

Characterization and Functional Significance of Calcium Transients in the 2-Cell Mouse Embryo Induced by an Autocrine Growth Factor

Emerson

Travis

Bathgate

et al. 2000

Journal of Biological Chemistry

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Growth of preimplantation embryos is influenced byThe cells of the mammalian preimplantation embryo (from the time of fertilization until the implantation of the blastocyst into the uterus) form the progenitor cells for all other cell lineages. The regulation of the growth and survival of the cells of the early embryo is, however, poorly understood. Mammalian preimplantation embryos develop in vitro with simple medium requirements and have no absolute requirement for exogenous vitamins, hormones, or growth factors. This contrasts with the absolute requirement of normal somatic cells for exogenous mitogens and survival factors. The continued mitoses of preimplantation embryo cells in the absence of exogenous growth factors implicates a role for endogenous, autocrine trophic factors, or the constitutive activation of signaling pathways in the early embryo. Several lines of evidence support a role for the former: (i) the rate of embryo development in vitro is density-dependent, with embryos growing in relatively small volumes (or in large groups) developing more successfully than those grown in large volumes (or individually) (1, 2); (ii) the synthesis by the preimplantation embryo of a number of growth factor ligands and their receptors (3-8); and (iii) the capacity of some exogenous growth factors to enhance embryo metabolism in vitro and to compensate for the adverse effects of culture in large medium volumes (1, 2, 9).Experimental partial deprivation of released autocrine trophic factors did not arrest the cell-cycle at given checkpoints (9). Rather, there was progressive loss of viability with increased cell death as embryos progressed past the 8-cell stage. This finding suggests that the autocrine factors may act as survival factors rather than classical growth factors (triggering progression through specific cell-cycle checkpoints). While several autocrine factors have been implicated, platelet-activating factor (PAF) 1 seems to be one of the first produced, being synthesized de novo by the embryo soon after fertilization (10, 11). Its actions are required by the mid-2-cell stage for normal rates of embryo survival (9).Despite this range of supportive data, there is limited direct evidence for the action of autocrine trophic factors in early embryo development. Transgenic and recombinant knock-out models have not generally been informative of the growth requirements of the early embryo prior to implantation. This may be due to extensive redundancy of regulatory pathways.

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confidence: 99%

Characterization and Functional Significance of Calcium Transients in the 2-Cell Mouse Embryo Induced by an Autocrine Growth Factor

Emerson

Travis

Bathgate

et al. 2000

Journal of Biological Chemistry

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“…Su et al confirmed that TRPV5 was highly expressed in the mouse blastocyst by microarray analysis [13], and we also verified its strong expression in blastocysts, whereas the level was undetectable in ES cells (data not shown). Ca 2+ is an essential signal for many cellular processes in embryogenesis, e.g., fertilization [14], cavitation [15,16], blastocoel formation [15] and blastocyst outgrowth [17][18][19]. Taken together, BSPRY-1 may be involved in cell differentiation and division in the early embryo via regulation of Ca 2+ influx with TPRV5, and it may be one reason why the activity level of the two isoforms of BSPRY is different in early embryo and ES cells.…”

Section: Discussionmentioning

confidence: 99%

B-box and SPRY Domain Containing Protein (BSPRY) is Associated with the Maintenance of Mouse Embryonic Stem Cell Pluripotency and Early Embryonic Development

Ikeda

Inoue

Ohkoshi

et al. 2012

Journal of Reproduction and Development

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Abstract. Mouse embryonic stem (ES) cells consist of heterogeneous populations with differing abilities to proliferate and differentiate. We previously demonstrated that the expression level of platelet endothelial cell adhesion molecule 1 (PECAM1)/CD31 was positively correlated with the undifferentiated state of mouse ES cells. In order to screen for a novel gene(s) involved in ES cell pluripotency, we performed an oligo microarray analysis and identified that B-box and SPRY domain containing protein (BSPRY) was expressed at high levels in PECAM1-positive cells. Two splice isoforms of BSPRY, BSPRY-1 and BSPRY-2, were expressed in undifferentiated ES cells and in blastocysts. Knockdown of BSPRY-1/2 in ES cells significantly reduced the number of undifferentiated colonies and caused increased expression of primitive ectoderm marker gene Fgf5. The overexpression of BSPRY-2 reciprocally increased the number of undifferentiated ES cells in the presence of LIF. Similarly, injection of BSPRY-1/2 siRNAs into 2-cell embryos caused developmental retardation and degeneration of embryos, and a significant decrease in the number of cells, especially in the inner cell mass (ICM), was observed at the blastocyst stage. Furthermore, microinjection of a BSPRY-1 expression vector into pronuclear stage embryos resulted in an increase in the hatching blastocysts rate after 120 h of culture. These results suggest that BSPRY-1 and BSPRY-2 are associated with both ES cell pluripotency and early embryonic development. E mbryonic stem (ES) cells are derived from the inner cell mass (ICM) of blastocysts and maintain the pluripotency to differentiate into three germ layers. Recent studies have demonstrated that mouse ES cells consist of heterogeneous populations with differing abilities to proliferate and differentiate [1][2][3]. We previously reported that there was wide variation in the expression of platelet endothelial cell adhesion molecule 1 (PECAM1) [1]. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis revealed that marker genes for undifferentiated ES cells were highly expressed in PECAM1-positive cells. PECAM1-positive ES cells injected into 8-cell host embryos could contribute to the epiblast in a chimeric embryo, but PECAM1-negative ES cells failed to differentiate into epiblast cells. These results suggested that the PECAM1 expression level was positively correlated with the undifferentiated state of ES cells.In order to search for a novel gene(s) involved in ES cell pluripotency, we analyzed gene expression profiles in PECAM1-positive and PECAM1-negative populations using an oligo microarray and isolated several genes that were expressed at high levels in PECAM1-positive cells. We focused upon one of these genes, which encodes mouse B-box and SPRY domain containing protein (BSPRY) protein, because in situ hybridization analysis revealed that Bspry was also expressed at the ICM of blastocysts [4]. These results suggest that BSPRY may be involved in not only ES cell pluripotency but also early emb...

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“…The ability of ethanol to accelerate development at dissimilar stages from the one-cell to the blastocyst stage suggests that ethanol may affect key developmental regulatory mechanisms. It therefore appears that there is a threshold concentration of ethanol for increasing intracellular calcium [16].…”

Section: Introductionmentioning

confidence: 98%

“…Last studies have indicated that ethanol can activate oocytes and causes parthenogenesis [16]- [18]. Ethanol with changing signaling pathway, controls the rate of embryogenesis and can affect the development of preimplantation stage embryos [19].…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore it was shown that the ethanol-mediated increase in intracellular Ca2+ is immediate and that a period of exposure of 5 min is as effective as exposure for 24 h in stimulating development [16], perhaps because ethanol initiates a signal-transduction cascade that has an impact on subsequent development. The ability of ethanol to accelerate development at dissimilar stages from the one-cell to the blastocyst stage suggests that ethanol may affect key developmental regulatory mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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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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Blastocyst Cavitation is Accelerated by Ethanol- or Ionophore-Induced Elevation of Intracellular Calcium1

Cited by 54 publications

References 54 publications

Characterization and Functional Significance of Calcium Transients in the 2-Cell Mouse Embryo Induced by an Autocrine Growth Factor

Characterization and Functional Significance of Calcium Transients in the 2-Cell Mouse Embryo Induced by an Autocrine Growth Factor

B-box and SPRY Domain Containing Protein (BSPRY) is Associated with the Maintenance of Mouse Embryonic Stem Cell Pluripotency and Early Embryonic Development

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

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