Trophinin-mediated cell adhesion induces apoptosis of human endometrial epithelial cells through PKC-δ

Tamura, Naoaki; Sato, Kazuhiro; Akama, Tomoya O.; Fukuda, Michiko N.

doi:10.4161/cc.10.1.14448

Cited by 27 publications

(20 citation statements)

References 40 publications

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“…After blastocyst attachment, the luminal epithelial cells surrounding the invading blastocyst undergo apoptosis (Parr et al, 1987; Schlafke et al, 1985; Welsh and Enders, 1991) to facilitate embryo invasion and access to maternal blood supply (Pampfer and Donnay, 1999; Parr et al, 1987). The apoptotic degeneration of the uterine epithelium involves embryo-derived signaling molecules, such as transforming growth factor β (Kamijo et al, 1998; Mahesh et al, 1996) and trophinin (Tamura et al, 2011), and is mediated by caspase 3 (Joswig et al, 2003; Zhang and Paria, 2006). Recent studies have demonstrated that KLF5, a zinc finger-containing transcription factor is primarily expressed in the luminal epithelium throughout the periimplantation stage (Ema et al, 2008; Sun et al, 2012).…”

Section: Molecular Basis Of Decidualizationmentioning

confidence: 99%

Physiological and molecular determinants of embryo implantation

Zhang

Lin

Kong

et al. 2013

Molecular Aspects of Medicine

450

480

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Embryo implantation involves the intimate interaction between an implantation-competent blastocyst and a receptive uterus, which occurs in a limited time period known as the window of implantation. Emerging evidence shows that defects originating during embryo implantation induce ripple effects with adverse consequences on later gestation events, highlighting the significance of this event for pregnancy success. Although a multitude of cellular events and molecular pathways involved in embryo-uterine crosstalk during implantation have been identified through gene expression studies and genetically engineered mouse models, a comprehensive understanding of the nature of embryo implantation is still missing. This review focuses on recent progress with particular attention to physiological and molecular determinants of blastocyst activation, uterine receptivity, blastocyst attachment and uterine decidualization. A better understanding of underlying mechanisms governing embryo implantation should generate new strategies to rectify implantation failure and improve pregnancy rates in women.

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Section: Molecular Basis Of Decidualizationmentioning

confidence: 99%

Physiological and molecular determinants of embryo implantation

Zhang

Lin

Kong

et al. 2013

Molecular Aspects of Medicine

450

480

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“…Binding of trophinin from an adjacent cell is predicted to dissociate bystin, thereby permitting phosphorylation of ErbB4 when heparin-binding epidermal-like growth factor (HB-EGF) is bound to ErbB4 (Sugihara et al, 2007). In trophectoderm, this produces a contactdependent proliferative signal, whereas -in epithelial cellshomophilic trans-ligation of trophinin induces tyrosine phosphorylation of protein kinase Cδ (PKCδ) and its translocation into the nucleus, which leads to apoptosis (Tamura et al, 2011). Wild-type mice blastocysts and uterus both express trophinin between 3.5 and 5.5 days post coitum but mice lacking it are fertile, so trophinin-mediated adhesion is dispensible at implantation (Nadano et al, 2002; please notice the comments on integrin knock-outs in Box 2).…”

Section: Trophinin and Hb-egfmentioning

confidence: 99%

Embryo–epithelium interactions during implantation at a glance

Aplin

Ruane

2017

Journal of Cell Science

198

140

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At implantation, with the acquisition of a receptive phenotype in the uterine epithelium, an initial tenuous attachment of embryonic trophectoderm initiates reorganisation of epithelial polarity to enable stable embryo attachment and the differentiation of invasive trophoblasts. In this Cell Science at a Glance article, we describe cellular and molecular events during the epithelial phase of implantation in rodent, drawing on morphological studies both in vivo and in vitro, and genetic models. Evidence is emerging for a repertoire of transcription factors downstream of the master steroidal regulators estrogen and progesterone that coordinate alterations in epithelial polarity, delivery of signals to the stroma and epithelial cell death or displacement. We discuss what is known of the cell interactions that occur during implantation, before considering specific adhesion molecules. We compare the rodent data with our much more limited knowledge of the human system, where direct mechanistic evidence is hard to obtain. In the accompanying poster, we represent the embryo-epithelium interactions in humans and laboratory rodents, highlighting similarities and differences, as well as depict some of the key cell biological events that enable interstitial implantation to occur.

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“…However, during the attachment reaction between the blastocyst and luminal epithelium, homophilic trophinin binding releases bystin, thus derepressing ERBB4, which can then become activated by HBEGF to promote trophoblast differentiation (Sugihara et al, 2007, Tamura et al, 2011. Meanwhile, in the luminal epithelium, homophilic trophinin binding disrupts its tethering of protein kinase Cδ to the plasma membrane, freeing the latter to enter the nucleus where it induces apoptosis (Tamura et al, 2011). Thus, trophinin signaling removes the cellular barrier to blastocyst implantation as it licenses activation of trophoblast adhesion competence.…”

Section: Human 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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Trophinin-mediated cell adhesion induces apoptosis of human endometrial epithelial cells through PKC-δ

Cited by 27 publications

References 40 publications

Physiological and molecular determinants of embryo implantation

Physiological and molecular determinants of embryo implantation

Embryo–epithelium interactions during implantation at a glance

Cell signaling in trophoblast-uterine communication

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