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

Stachecki, James J.; Armant, D. Randall

doi:10.1095/biolreprod55.6.1292

Cited by 34 publications

(27 citation statements)

References 47 publications

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“…The fact that U 73122 and neomycin significantly blocked EGF-induced stimulation of 2-DG uptake indicates that PLC has a controlling role of glucose uptake in mouse ES cells. As ES cells are derived from the inner cell mass of the blastocyst, this work on the effect of PLC inhibition in ES cells is in agreement with the work of Stachecki and Armant [41] showing that the regulation of blastocyst formation in mice is mediated through a PLC-dependent pathway that can be inhibited by U 73122.…”

Section: A B a Bsupporting

confidence: 89%

PKC and MAPKs Pathways Mediate EGF-induced Stimulation of 2-Deoxyglucose Uptake in Mouse Embryonic Stem Cells

Heo

Han

2006

Cell Physiol Biochem

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It has been reported that epidermal growth factor (EGF) and EGF receptor were highly expressed in embryo, suggesting that the EGF system is related to early embryo development in an autocrine and/or paracrine manner. Glucose becomes the preimplantation exogenous energy substrate and enters the blastocyst via glucose transporters. Thus, the effect of EGF on [3H]-2-deoxyglucose (2-DG) uptake and its related signaling pathways were examined in mouse embryonic stem (ES) cells. EGF significantly increased 2-DG uptake in time- and concentration- dependent manner (>12 hr, >10 ng/ ml) and increased mRNA and protein level of glucose transporter 1 (GLUT1) compared to control, respectively. Actinomycin D and cycloheximide completely blocked the effect of EGF on 2-DG uptake. EGF-induced increase of 2-DG uptake was blocked by AG1478 (EGF receptor tyrosine kinase blocker), genistein or herbimycin (tyrosine kinase inhibitors). In addition, EGF effect was blocked by neomycin and U 73122 [phospholipase C (PLC) inhibitors] as well as staurosporine and bisindolylmaleimide I [protein kinase C (PKC) inhibitors]. EGF was also observed to increase inositol phosphates (IPs) formation and activate a PKC translocation from the cytosolic to membrane fraction, suggesting a role of PLC and PKC. SB 203580 [p38 mitogen activated protein kinase (MAPK) inhibitor] or PD 98059 (p44/42 MAPKs inhibitor) blocked EGF-induced increase of 2-DG uptake. EGF also increased phosphorylation of p38 MAPK and p44/42 MAPKs, which was blocked by genistein or bisindolylmaleimide I, respectively. In conclusion, EGF partially increased 2-DG uptake via PKC, p38 MAPK, and p44/42 MAPKs in mouse ES cells.

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Section: A B a Bsupporting

confidence: 89%

PKC and MAPKs Pathways Mediate EGF-induced Stimulation of 2-Deoxyglucose Uptake in Mouse Embryonic Stem Cells

Heo

Han

2006

Cell Physiol Biochem

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“…Lysophosphatidic acid (LPA) produced in the maternal reproductive tract accelerates blastocoel formation at the morula stage and trophoblast differentiation at the early blastocyst stage through downstream intracellular Ca 2+ signaling (Liu andArmant, 2004, Stachecki andArmant, 1996). LPA activates cognate G protein-coupled receptors that signal through phospholipase C to generate inositol-1,4,5-trisphosphate and diacylglycerol that, in turn, mobilize cytoplasmic free Ca 2+ and activate protein kinase C (PKC), respectively (Contos et al, 2000).…”

Section: Mouse Implantationmentioning

confidence: 99%

Cell signaling in trophoblast-uterine communication

Fritz¹,

Jain²,

Armant³

2014

Int. J. Dev. Biol.

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Intricate and precise communication between the blastocyst and the uterus orchestrates embryo implantation. However, many questions remain unanswered regarding the molecular complexities of implantation. On-time implantation requires a receptive uterus and a mature blastocyst with trophoblast cells capable of adhering to and invading the endometrium. Defects in uterine receptivity or embryo/uterine signaling can cause implantation failure or early pregnancy loss, whereas deficient trophoblast differentiation can generate placental abnormalities that produce adverse pregnancy outcomes. This review will discuss several examples of signaling pathways that regulate trophoblast and uterine development during this period. Leukemia inhibitory factor is involved in uterine priming for implantation. The epidermal growth factor signaling system contributes to trophoblast-uterine communication, as well as trophoblast adhesion and invasion. Indian hedgehog signaling synchronizes tissue compartments within the uterus, and WNT signaling mediates numerous interactions within the implantation site and developing placenta. The autocrine, paracrine and juxtacrine interactions mediated by these signaling pathways contribute significantly to the establishment of pregnancy, although there are many other known and yet to be discovered factors that synchronize the maternal and embryonic developmental programs.

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“…PKC a may be involved in compaction, since it redistributes to contact sites as compaction initiates and can phosphorylate b-catenin (Pauken & Capco 1999). It has also been demonstrated that blastocoele formation is regulated through phospholipase C (an enzyme that is known to activate PKCdependent pathways; Stachecki & Armant 1996), and that targeted disruption of mouse phospholipase Cb3 (the most widely expressed member of the phospholipase Cb family) results in early preimplantation death (Wang et al 1998). Although all of these studies suggest a role for the PKC family in preimplantation development, the relative importance of each isozyme is unknown.…”

Section: Introductionmentioning

confidence: 99%

Expression profile of protein kinase C isozymes in preimplantation mouse development

Dehghani¹,

Hahnel²

2005

Reproduction

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In the preimplantation mouse embryo, the protein kinase C (PKC) family has been implicated in regulation of egg activation, progression of meiotic and mitotic cell cycles, embryo compaction, and blastulation, but the involvement of the individual isozymes is largely unknown. Here, using semiquantitative immunocytochemistry and confocal microscopy we analyze the relative amount and subcellular distribution of ten isozymes of PKC (a, bI, bII, g, d, 1, h, u, z, i/l) and a PKC-anchoring protein, receptor for activated C-kinase 1 (RACK1). Our results show that all of these isoforms of PKC are present between the twocell and blastocyst stages of mouse preimplantation development, and that each has a distinct, dynamic pattern and level of expression. The data suggest that different complements of the isozymes are involved in various steps of preimplantation development, and will serve as a framework for further functional studies of the individual isozymes. In particular, there was a transient increase in the nuclear concentration of several isozymes at the early four-cell stage, suggesting that some of the PKC isozymes might be involved in regulation of nuclear organization and function in the early mouse embryo.

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

Cited by 34 publications

References 47 publications

PKC and MAPKs Pathways Mediate EGF-induced Stimulation of 2-Deoxyglucose Uptake in Mouse Embryonic Stem Cells

PKC and MAPKs Pathways Mediate EGF-induced Stimulation of 2-Deoxyglucose Uptake in Mouse Embryonic Stem Cells

Cell signaling in trophoblast-uterine communication

Expression profile of protein kinase C isozymes in preimplantation mouse development

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