scholarly journals Hormone Excretion and Peroxisomes of Human Immortalized Extravillous Trophoblast Cells (TCL-2) Derived from First-Trimester Placenta

2009 ◽  
Vol 129 (11) ◽  
pp. 1423-1430
Author(s):  
Fumie HASHIMOTO ◽  
Asuka ONO ◽  
Kikumi MATSUOKA ◽  
Sadaki YOKOTA ◽  
Hiroyuki SEKI ◽  
...  
Keyword(s):  
First Trimester ◽  
Extravillous Trophoblast ◽  
Trophoblast Cells ◽  
Hormone Excretion

scholarly journals Blocking Epidermal Growth Factor Receptor Signaling in HTR-8/SVneo First Trimester Trophoblast Cells Results in Dephosphorylation of PKBα/AKT and Induces Apoptosis

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
J. Bolnick ◽  
L. Albitar ◽  
L. L. Laidler ◽  
R. Abdullah ◽  
K. K. Leslie
Keyword(s):  
Protein Phosphorylation ◽  
Global Analysis ◽  
Growth Factor Receptor ◽  
First Trimester ◽  
Extravillous Trophoblast ◽  
Signaling Proteins ◽  
Trophoblast Cells ◽  
Novel Technology ◽  
Epidermal Growth ◽  
Growth Factor Receptor Signaling

We identified a major peptide signaling target of EGF/EGFR pathway and explored the consequences of blocking or activating this pathway in the first trimester extravillous trophoblast cells, HTR-8/SVneo. A global analysis of protein phosphorylation was undertaken using novel technology (Kinexus Kinetworks) that utilizes SDS-polyacrylamide minigel electrophoresis and multi-lane immunoblotting to permit specific and semiquantitative detection of multiple phosphoproteins. Forty-seven protein phosphorylation sites were queried, and the results reported based on relative phosphorylation at each site. EGF- and Iressa-(gefitinib, ZD1839, an inhibitor of EGFR) treated HTR-8/SVneo cells were subjected to immunoblotting and flow cytometry to confirm the phosphoprotein screen and to assess the effects of EGF versus Iressa on cell cycle and apoptosis. EGFR mediates the phosphorylation of important signaling proteins, including PKBα/AKT. This pathway is likely to be central to EGFR-mediated trophoblast survival. Furthermore, EGF treatment induces proliferation and inhibits apoptosis, while Iressa induces apoptosis.

scholarly journals Reconstructing the human first trimester fetal–maternal interface using single cell transcriptomics

2018 ◽  
Author(s):  
Roser Vento-Tormo ◽  
Mirjana Efremova ◽  
Rachel A. Botting ◽  
Margherita Y. Turco ◽  
Miquel Vento-Tormo ◽  
...  
Keyword(s):  
Nk Cells ◽  
Single Cell ◽  
Single Cells ◽  
First Trimester ◽  
Maternal Blood ◽  
Extravillous Trophoblast ◽  
Trophoblast Cells ◽  
Hormone Production ◽  
Statistical Tool ◽  
Uterine Mucosa

SummaryDuring the early weeks of human pregnancy, the fetal placenta implants into the uterine mucosa (decidua) where placental trophoblast cells intermingle and communicate with maternal cells. Here, we profile transcriptomes of ∼50,000 single cells from this unique microenvironment, sampling matched first trimester maternal blood and decidua, and fetal cells from the placenta itself. We define the cellular composition of human decidua, revealing five distinct subsets of decidual fibroblasts with differing growth factors and hormone production profiles, and show that fibroblast states define two distinct decidual layers. Among decidual NK cells, we resolve three subsets, each with a different immunomodulatory and chemokine profile. We develop a repository of ligand-receptor pairs (www.CellPhoneDB.org) and a statistical tool to predict the probability of cell-cell interactions via these pairs, highlighting specific interactions between decidual NK cells and invading fetal extravillous trophoblast cells, maternal immune and stromal cells. Our single cell atlas of the maternal-fetal interface reveals the cellular organization and interactions critical for placentation and reproductive success.

Plasma from first trimester pre-symptomatic women who subsequently developed preeclampsia reduces extravillous trophoblast cells migration, a possible role of placental-derived particles

Placenta ◽  
2014 ◽  
Vol 35 (9) ◽  
pp. A83 ◽  
Author(s):  
Carlos Salomon ◽  
Sarah Yee ◽  
Suchismita Sarker ◽  
Katherin Scholz-Romero ◽  
Sebastian Illanes ◽  
...  
Keyword(s):  
First Trimester ◽  
Extravillous Trophoblast ◽  
Trophoblast Cells

The expression of ADAM (a Disintegrin and Metalloproteinase) genes in human first-trimester villous and extravillous trophoblast cells

Placenta ◽  
2015 ◽  
Vol 36 (9) ◽  
pp. A22
Author(s):  
Hironori Takahashi ◽  
Dongwei Zhao ◽  
Akihide Ohkuchi ◽  
Shigeki Matsubara ◽  
Toshihiro Takizawa
Keyword(s):  
First Trimester ◽  
Extravillous Trophoblast ◽  
Trophoblast Cells ◽  
A Disintegrin And Metalloproteinase

scholarly journals Aberrant TGFβ Signaling Contributes to Altered Trophoblast Differentiation in Preeclampsia

Endocrinology ◽  
2015 ◽  
Vol 157 (2) ◽  
pp. 883-899 ◽  
Author(s):  
Jing Xu ◽  
Tharini Sivasubramaniyam ◽  
Yoav Yinon ◽  
Andrea Tagliaferro ◽  
Jocelyn Ray ◽  
...  
Keyword(s):  
Intracellular Signaling ◽  
Late Onset ◽  
First Trimester ◽  
Extravillous Trophoblast ◽  
Cell Cycle Regulators ◽  
Trophoblast Cells ◽  
Tgfβ Signaling ◽  
Aberrant Expression ◽  
Smad2 Phosphorylation ◽  
Tgfβ Receptor

Abstract TGFβ has been implicated in preeclampsia, but its intracellular signaling via phosphorylated mothers against decapentaplegic (SMADs) and SMAD-independent proteins in the placenta remains elusive. Here we show that TGFβ receptor-regulated SMAD2 was activated (Ser465/467 phosphorylation) in syncytiotrophoblast and proliferating extravillous trophoblast cells of first-trimester placenta, whereas inhibitory SMAD7 located primarily to cytotrophoblast cells. SMAD2 phosphorylation decreased with advancing gestation, whereas SMAD7 expression increased and shifted to syncytiotrophoblasts toward term. Additionally, we found that the TGFβ SMAD-independent signaling via partitioning defective protein 6 (PARD6)/Smad ubiquitylation regulatory factor was activated at approximately 10–12 weeks of gestation in cytotrophoblast and extravillous trophoblast cells comprising the anchoring column. Placentae from early-onset, but not late-onset, preeclampsia exhibited elevated SMAD2 phosphorylation and SMAD7 levels. Whereas PARD6 expression increased and SMURF1 levels decreased in preeclamptic placentae, their association increased. SMAD2 phosphorylation by TGFβ in villous explants and BeWo cells resulted in a reduction of Glial cell missing-1 (GCM1) and fusogenic protein syncytin-1 while increasing cell cycle regulators cyclin E-1 (CCNE1) and cyclin-dependent kinase 4. SMAD7 abrogated the proliferative effects of TGFβ. CCNE1 levels were increased in preeclamptic placentae, whereas GCM1 was markedly reduced. In addition, TGFβ treatment increased the association of PARD6 and SMURF1 and down-regulated Ras homolog gene family, member A (RHOA) GTPase in JEG3 cells. In a wound assay, TGFβ treatment increased the association of PARD6 and SMURF1 and triggered JEG3 cell migration through increased cellular protrusions. Taken together, our data indicate that TGFβ signaling via both SMAD2/7 and PARD6/SMURF1 pathways plays a role in trophoblast growth and differentiation. Altered SMAD regulation of GCM1 and CCNE1 and aberrant expression/activation of PARD6/SMURF1 may contribute to the pathogenesis of preeclampsia by affecting cellular pathways associated with this disorder.

scholarly journals The BMP2 Signaling Axis Promotes Invasive Differentiation of Human Trophoblasts

2021 ◽  
Vol 9 ◽  
Author(s):  
Jiali You ◽  
Wei Wang ◽  
Hsun-Ming Chang ◽  
Yuyin Yi ◽  
Hongjin Zhao ◽  
...  
Keyword(s):  
Embryo Implantation ◽  
First Trimester ◽  
Limiting Factors ◽  
Extravillous Trophoblast ◽  
Trophoblast Invasion ◽  
Cell Marker ◽  
Trophoblast Cells ◽  
Trophoblast Stem Cells ◽  
Signaling Axis ◽  
First Trimester Of Pregnancy

Embryo implantation and trophoblast invasion are principal limiting factors of pregnancy establishment. Aberrant embryo development or improper trophoblast differentiation and invasion may lead to various unfavorable pregnancy-related outcomes, including early pregnancy loss (EPL). Our clinical data show that the serum BMP2 levels were significantly increased during the first trimester of pregnancy and that the serum and BMP2 expression levels were lower in women with EPL than in women with normal early pregnancies. Moreover, we observed that BMP2 was expressed in oocytes and trophoblast cells of cleaved embryos and blastocysts prior to implantation in both humans and mice. Exogenous BMP2 promoted embryonic development by enhancing blastocyst formation and hatching in mice. LncRNA NR026833.1 was upregulated by BMP2 and promoted SNAIL expression by competitively binding to miR-502-5p. SNAIL induced MMP2 expression and promoted cell invasion in primary extravillous trophoblast cells. BMP2 promotes the invasive differentiation of mouse trophoblast stem cells by downregulating the expression of TS cell marker and upregulating the expression of trophoblast giant cell marker and labyrinthine/spongiotrophoblast marker. Our findings provide significant insights into the regulatory roles of BMP2 in the development of the placenta, which may give us a framework to explore new therapeutic strategies to pregnancy-related complications.

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