Prolactin stimulates cell migration and invasion by human trophoblast in vitro

Stefanoska, Ivana; Krivokuća, Milica Jovanović; Vasilijic, S.; Ćujić, Danica; Vićovac, Ljiljana

doi:10.1016/j.placenta.2013.06.305

Cited by 56 publications

(34 citation statements)

References 54 publications

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“…A defining feature of EVT differentiation is upregulation of the non-classical MHC class I molecule HLA-G, as well as HLA-C (King et al, 1996(King et al, , 2000bKovats et al, 1990). The expression of several growth factor receptors also changes: EGFR, MET (the receptor for HGF), prolactin receptor (PRLR) and the BMP receptor BMPR1A are downregulated, while ERBB2 is upregulated (Jokhi et al, 1994;Kauma et al, 1999;Ladines-Llave et al, 2013;Stefanoska et al, 2013;Tilburgs et al, 2015). All of these changes are accompanied by loss of proliferation, as assessed by Ki67 expression, and a change in expression of cell cycle regulators (Chan et al, 1999;Genbacev et al, 2000).…”

Section: Evt Differentiationmentioning

confidence: 99%

Development of the human placenta

2019

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The placenta is essential for normal in utero development in mammals. In humans, defective placental formation underpins common pregnancy disorders such as pre-eclampsia and fetal growth restriction. The great variation in placental types across mammals means that animal models have been of limited use in understanding human placental development. However, new tools for studying human placental development, including 3D organoids, stem cell culture systems and single cell RNA sequencing, have brought new insights into this field. Here, we review the morphological, molecular and functional aspects of human placental formation, with a focus on the defining cell of the placentathe trophoblast.

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Section: Evt Differentiationmentioning

confidence: 99%

Development of the human placenta

2019

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“…In our experiments, TPPP3 knockdown in hESCs resulted in decreased prolactin and IGFBP-1 protein level, compared to control group during decidualization. Both decidual prolactin and IGFBP-1 act as endocrine and autocrine/paracrine factors and are believed to play an important role at the blastocyst-maternal interface in the regulation of implantation and pregnancy (Irwin et al 2001, Jabbour & Critchley 2001, Stefanoska et al 2013, Gellersen & Brosens 2014.…”

Section: Figurementioning

confidence: 99%

Inhibition of TPPP3 attenuates β-catenin/NF-κB/COX-2 signaling in endometrial stromal cells and impairs decidualization

Shukla

Kaushal

Sankhwar

et al. 2019

Journal of Endocrinology

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Embryo implantation and decidualization are critical events that occur during early pregnancy. Decidualization is synchronized by the crosstalk of progesterone and the cAMP signaling pathway. Previously, we confirmed the role of TPPP3 during embryo implantation in mice, but the underlying role and mechanism of TPPP3 in decidualization has not yet been understood. The current study was aimed to investigate the role of TPPP3 in decidualizationin vivoandin vitro. Forin vivoexperiments, decidual reaction was artificially induced in the uteri of BALB/c mice. TPPP3 was found to be highly expressed during decidualization, whereas in the uteri receiving TPPP3 siRNA, decidualization was suppressed and the expression of β-catenin and decidual marker prolactin was reduced. In human endometrium, TPPP3 protein was found to be predominantly expressed in the mid-secretory phase (LH+7). In the primary culture of human endometrial stromal cells (hESCs), TPPP3 siRNA knockdown inhibited stromal-to-decidual cell transition and decreased the expression of the decidualization markers prolactin andIGFBP-1. Immunofluorescence and immunoblotting experiments revealed that TPPP3 siRNA knockdown suppressed the expression of β-catenin, NF-κB and COX-2 in hESCs during decidualization. TPPP3 inhibition also decreased NF-kB nuclear accumulation in hESCs and suppressed NF-κB transcriptional promoter activity. COX-2 expression was significantly decreased in the presence of a selective NF-kB inhibitor (QNZ) implicating that NF-kB is involved in COX-2 expression in hESCs undergoing decidualization. TUNEL assay and FACS analysis revealed that TPPP3 knockdown induced apoptosis and caused loss of mitochondrial membrane potential in hESCs. The study suggested that TPPP3 plays a significant role in decidualization and its inhibition leads to the suppression of β-catenin/NF-κB/COX-2 signaling along with the induction of mitochondria-dependent apoptosis.

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“…It has also been documented that the schCTBs and the placental cell column CTBs have similar composition of the extracellular matrix [15, 16], produce similar sets of cytokines [17, 18], and express prolactin receptors (Vicovac, unpublished results) and EGFR [19]. Both prolactin [20] and EGF [21] have been shown to stimulate invasion of the CTBs in vitro . At the functional level, as revealed in the standard invasion assay with Matrigel coated porous membranes, 16–18 weeks schCTBs were more invasive in vitro than placental CTBs from the same specimen (Genbacev, unpublished results).…”

Section: Development Of the Chorionmentioning

confidence: 99%

The role of chorionic cytotrophoblasts in the smooth chorion fusion with parietal decidua

2015

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Human placenta and chorion are rapidly growing transient embryonic organs built from diverse cell populations that are of either, ectodermal [placenta and chorion specific trophoblast (TB) cells], or mesodermal origin [villous core and chorionic mesenchyme]. The development of placenta and chorion is synchronized from the earliest phase of implantation. Little is known about the formative stages of the human chorion, in particular the steps between the formation of a smooth chorion and its fusion with the parietal decidua. Here, we provided evidence that the mechanism by which smooth chorion fuses with parietal decidua is the invasion of smooth chorionic cytotrophoblasts (schCTBs) into the uterine wall opposite to the implantation side. This process, which partially replicates some of the mechanisms of the blastocyst implantation, leads to the formation of a new zone of contacts between fetal and maternal cells. We further analyzed the characteristics of the recently established human self-renewing trophoblast progenitor cells (TBPC), derived from chorionic mesoderm, and we propose the mechanism by which they might in vivo contribute to the pool of the invasive schCTBs.

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Prolactin stimulates cell migration and invasion by human trophoblast in vitro

Cited by 56 publications

References 54 publications

Development of the human placenta

Development of the human placenta

Inhibition of TPPP3 attenuates β-catenin/NF-κB/COX-2 signaling in endometrial stromal cells and impairs decidualization

The role of chorionic cytotrophoblasts in the smooth chorion fusion with parietal decidua

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