Cell signaling in trophoblast-uterine communication

Fritz, Rani; Jain, Chandni; Armant, D. Randall

doi:10.1387/ijdb.140011da

Cited by 66 publications

(66 citation statements)

References 133 publications

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“…EG‐VEGF is a critical factor in embryo implantation and placental development. In addition, an enhanced trophoblast invasion ability promotes the process of embryo implantation (Fritz et al, ). However, whether EG‐VEGF facilitates trophoblast invasion, and what the underlying signaling mechanism might be, have been unclear.…”

Section: Resultsmentioning

confidence: 99%

Primary Cilium‐Regulated EG‐VEGF Signaling Facilitates Trophoblast Invasion

Wang

Tsai

Syu

et al. 2016

Journal Cellular Physiology

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Trophoblast invasion is an important event in embryo implantation and placental development. During these processes, endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is the key regulator mediating the crosstalk at the feto-maternal interface. The primary cilium is a cellular antenna receiving environmental signals and is crucial for proper development. However, little is known regarding the role of the primary cilium in early human pregnancy. Here, we demonstrate that EG-VEGF regulates trophoblast cell invasion via primary cilia. We found that EG-VEGF activated ERK1/2 signaling and subsequent upregulation of MMP2 and MMP9, thereby facilitating cell invasion in human trophoblast HTR-8/SVneo cells. Inhibition of ERK1/2 alleviated the expression of MMPs and trophoblast cell invasion after EG-VEGF treatment. In addition, primary cilia were observed in all the trophoblast cell lines tested and, more importantly, in human first-trimester placental tissue. The receptor of EG-VEGF, PROKR1, was detected in primary cilia. Depletion of IFT88, the intraflagellar transporter required for ciliogenesis, inhibited primary cilium growth, thereby ameliorating ERK1/2 activation, MMP upregulation, and trophoblast cell invasion promoted by EG-VEGF. These findings demonstrate a novel function of primary cilia in controlling EG-VEGF-regulated trophoblast invasion and reveal the underlying molecular mechanism. J. Cell. Physiol. 232: 1467-1477, 2017. © 2016 Wiley Periodicals, Inc.

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Section: Resultsmentioning

confidence: 99%

Primary Cilium‐Regulated EG‐VEGF Signaling Facilitates Trophoblast Invasion

Wang

Tsai

Syu

et al. 2016

Journal Cellular Physiology

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“…38,43 Collectively, these studies provide evidence of EGF and it receptors as important regulators of trophoblast cells. 44 …”

Section: Inducers Of Emtmentioning

confidence: 99%

Epithelial-mesenchymal transition during extravillous trophoblast differentiation

Davies

Pollheimer

Yong

et al. 2016

Cell Adhesion & Migration

209

146

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A successful pregnancy depends on the intricate and timely interactions of maternal and fetal cells. Placental extravillous cytotrophoblast invasion involves a cellular transition from an epithelial to mesenchymal phenotype. Villous cytotrophoblasts undergo a partial epithelial to mesenchymal transition (EMT) when differentiating into extravillous cytotrophoblasts and gain the capacity to migrate and invade. This review summarizes our current knowledge regarding known regulators of EMT in the human placenta, including the inducers of EMT, upstream transcription factors that control EMT and the downstream effectors, cell adhesion molecules and their differential expression and functions in pregnancy pathologies, preeclampsia (PE) and fetal growth restriction (FGR). The review also describes the research strategies that were used for the identification of the functional role of EMT targets in vitro. A better understanding of molecular pathways driven by placental EMT and further elucidation of signaling pathways underlying the developmental programs may offer novel strategies of targeted therapy for improving feto-placental growth in placental pathologies including PE and FGR.

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“…Before they physically connect, both have been suggested to already secrete a wide variety of signals, the so-called embryo-endometrium crosstalk, which includes hormones, growth factors and cytokines 16, 17 . After embedding into uterine epithelial and stromal cells, paracrine and cellular signaling has been suggested to further steer the progress of implantation 18, 19 .…”

Section: Introductionmentioning

confidence: 99%

High-quality human preimplantation embryos stimulate endometrial stromal cell migration via secretion of microRNA hsa-miR-320a

Berkhout

Keijser

Repping

et al. 2020

Preprint

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Implantation failure is one of the major success limiting factors in human reproduction. Despite, the mechanisms that determine successful human embryo implantation remain largely unknown. We here show that high-quality human preimplantation embryos secrete soluble signaling factors, including micro RNA (miRNA) hsa-miR-320a, that promote migration of human endometrial stromal cells (hESCs). By using miRNA mimics and inhibitors, we demonstrate that hsa-miR-320a alone can stimulate migration of decidualized hESCs, accurately resembling the response typically triggered only by high-quality embryos. Transcriptome analysis further demonstrated that this effect is very likely mediated via altered expression of genes involved in cell adhesion and cytoskeleton organization. In conclusion, by secreting hsa-miR-320a, high-quality human preimplantation embryos directly influence endometrial stromal cells, most likely to prime the endometrium at the implantation site for successful implantation. Together, our results indicate that hsa-miR-320a may be a promising target to further increase success rates in assisted reproduction.

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Cell signaling in trophoblast-uterine communication

Cited by 66 publications

References 133 publications

Primary Cilium‐Regulated EG‐VEGF Signaling Facilitates Trophoblast Invasion

Primary Cilium‐Regulated EG‐VEGF Signaling Facilitates Trophoblast Invasion

Epithelial-mesenchymal transition during extravillous trophoblast differentiation

High-quality human preimplantation embryos stimulate endometrial stromal cell migration via secretion of microRNA hsa-miR-320a

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