scholarly journals The Downregulation of Placental Lumican Promotes the Progression of Preeclampsia

2021 ◽  
Author(s):  
Chao Liu ◽  
Yulian Hu ◽  
Zhongying Wang ◽  
Hua Pan ◽  
Yan Ren ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Line ◽  
Control Group ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
P53 Expression ◽  
Fluorescence Quantitative Pcr ◽  
And Migration ◽  
Negative Controls ◽  
The Impact

AbstractMultiple pieces of evidence illustrate that impaired trophoblast function results in preeclampsia (PE), and migration/invasion of human trophoblast cells is stringently regulated by extracellular matrix (ECM) components. Many studies have indicated abnormal expressions of placental ECM components are associated with preeclampsia. However, the change and influence of lumican, a vital member of extracellular matrix (ECM) molecules, on trophoblast cells during preeclampsia remain unclear. This study examines the possibility that the roles of lumican in trophoblast cells contribute to PE. To address this issue, the expression of lumican in human placental tissues was observed using immunohistochemistry, fluorescence quantitative PCR, and Western blot technology. After the HTR-8/SVneo cell line was transfected with pcDNA3.1-human lumican, pGPU6-human lumican shRNA, and their negative controls, the impact of lumican on the HTR-8/SVneo cell line was investigated. Lumican was expressed in human placental tissues. Compared with the control group, its expression was significantly lower in PE placentas. Lumican downregulation inhibited cell proliferation significantly and reduced Bcl-2 expression, but increased P53 expression. These results indicate that the downregulation of placental lumican may drive PE development via promoting the downregulation of Bcl-2 expression and upregulation of P53.

213. Chemokines: key players at the maternal - fetal interface

2008 ◽  
Vol 20 (9) ◽  
pp. 13
Author(s):  
N. J. Hannan ◽  
L. A. Salamonsen
Keyword(s):  
Extracellular Matrix ◽  
Real Time ◽  
Extracellular Matrix Protein ◽  
Leukocyte Trafficking ◽  
Trophoblast Cells ◽  
Rt Pcr ◽  
Human Trophoblast ◽  
Decidual Cells ◽  
Trophoblast Migration ◽  
Maternal Fetal Interface

Establishment of pregnancy requires extensive communication at the maternal-fetal interface and involves a plethora of locally acting molecules, including the chemokines. Chemokines are multifunctional molecules initially described for roles in leukocyte trafficking, but since found to participate in many other processes such as differentiation and directed migration. Previously we have shown that the chemokines, CX3CL1 and CCL14, are abundant in human endometrial vasculature, leukocytes, epithelial and decidual cells at the time of implantation and that their receptors, CX3CR1 and CCR1, are present on invading human trophoblast. CX3CL1 and CCL14 directly promote human trophoblast migration. We hypothesised that these endometrial chemokines promote trophoblast migration by regulating adhesion molecules and extracellular matrix (ECM) components on the trophoblast, similar to mechanisms used in leukocyte trafficking. Trophoblast cells (AC1M-88) used previously, showed a marked increase in adhesion to fibronectin following treatment with CX3CL1 and CCL14. Alterations in trophoblast adhesion associated and ECM genes following chemokine stimulation were examined using pathway specific oligo-arrays and quantitative real-time RT–PCR. Over 30 transcripts were affected by CX3CL1 treatment and 15 were regulated by CCL14 treatment. Real-time RT–PCR confirmed significant changes in the mRNA transcripts of α-catenin (CTNNA1), extracellular matrix protein-1 (ECM1), osteopontin (SPP1), integrin α6 (ITGA6), matrix metalloproteinase-12 (MMP12) and integrin β5 (ITGB5) following chemokine treatment. Several of these molecules have previously been implicated in implantation. Immunohistochemistry confirmed the presence of integrin α6, SPP1 and ECM1 protein in first trimester human implantation sites. The temporal and spatial expression of chemokines, their receptors and adhesion related molecules at the maternal-fetal interface emphasises an important role in the controlled directional migration of trophoblast through the maternal decidua. For the first time this study demonstrates direct effects of CX3CL1 and CCL14 on trophoblast adhesion and ECM molecules suggesting mechanisms by which trophoblast cells migrate during early pregnancy.

scholarly journals Autocrine and Paracrine Mechanisms of Prostaglandin E2 Action on Trophoblast/Conceptus Cells through the Prostaglandin E2 Receptor (PTGER2) during Implantation

Endocrinology ◽  
2013 ◽  
Vol 154 (10) ◽  
pp. 3864-3876 ◽  
Author(s):  
Agnieszka Waclawik ◽  
Piotr Kaczynski ◽  
Henry N. Jabbour
Keyword(s):  
Extracellular Matrix ◽  
Cell Adhesion ◽  
Prostaglandin E2 ◽  
Mapk Signaling ◽  
Intercellular Adhesion Molecule ◽  
Pcr Analysis ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Uterine Lumen ◽  
Estradiol 17Β

The conceptus and endometrium secrete large amounts of prostaglandin E2 (PGE2) into the porcine uterine lumen during the periimplantation period. We hypothesized that PGE2 acts on conceptus/trophoblast cells through auto- and paracrine mechanisms. Real-time RT-PCR analysis revealed that PGE2 receptor (PTGER)2 mRNA was 14-fold greater in conceptuses/trophoblasts on days 14–25 (implantation and early placentation period) vs preimplantation day 10–13 conceptuses (P < .05). Similarly, expression of PTGER2 protein increased during implantation. Conceptus expression of PTGER4 mRNA and protein did not differ on days 10–19. PGE2 stimulated PTGER2 mRNA expression in day 15 trophoblast cells through PTGER2 receptor signaling. PGE2 elevated aromatase expression and estradiol-17β secretion by trophoblast cells. Moreover, PGE2 and the PTGER2 agonist, butaprost, increased the adhesive capacity of both human HTR-8/SVneo trophoblast and primary porcine trophoblast cells to extracellular matrix. This PGE2-induced alteration in trophoblast cell adhesion to extracellular matrix was abolished by incubation of these cells with AH6809 (PTGER2 antagonist), ITGAVB3-directed tetrapeptide arg-gly-asp-ser or integrin ITGAVB3 antibody. PGE2 stimulated adhesion of porcine trophoblast cells via the estrogen receptor and MEK/MAPK signaling pathway. PGE2 induced phosphorylation of MAPK1/MAPK3 through PTGER2 and up-regulated expression of cell adhesion proteins such as focal adhesion kinase and intercellular adhesion molecule-1. Our study indicates that elevated PGE2 in the periimplantation uterine lumen stimulates conceptus PTGER2 expression, which in turn promotes trophoblast adhesion via integrins, and synthesis and secretion of the porcine embryonic signal estradiol-17β. Moreover, the mechanism through which PGE2 increases trophoblast adhesion is not species specific because it is PTGER2- and integrin-dependent in both porcine and human trophoblast cells.

Differentiation of human trophoblast cells in vitro stimulated by extracellular matrix

Placenta ◽  
1993 ◽  
Vol 14 ◽  
pp. 181-200
Author(s):  
Hans-Peter Hohn ◽  
Larry R. Boots ◽  
Hans-Werner Denker ◽  
Magnus Höök
Keyword(s):  
Extracellular Matrix ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Human Trophoblast Cells

Role of extracellular matrix in regulation of type IV collagenase synthesis by human trophoblast cells and their malignant counterparts

Placenta ◽  
1993 ◽  
Vol 14 ◽  
pp. 201-210
Author(s):  
Hervé Emonard ◽  
Maryam Aghayan ◽  
Monique Smet ◽  
Jean-Pierre Schaaps ◽  
Jean-Alexis Grimaud ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Trophoblast Cells ◽  
Type Iv Collagenase ◽  
Human Trophoblast ◽  
Type Iv ◽  
Human Trophoblast Cells

scholarly journals The Cytokine Gene CXCL14 Restricts Human Trophoblast Cell Invasion by Suppressing Gelatinase Activity

Endocrinology ◽  
2009 ◽  
Vol 150 (12) ◽  
pp. 5596-5605 ◽  
Author(s):  
HaiBin Kuang ◽  
Qi Chen ◽  
Ying Zhang ◽  
Li Zhang ◽  
HongYing Peng ◽  
...  
Keyword(s):  
Trophoblast Cell ◽  
Trophoblast Invasion ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Gelatinase Activity ◽  
Invasion And Migration ◽  
Human Pregnancy ◽  
Decidual Cells ◽  
And Migration ◽  
Maternal Fetal Interface

Abstract Well-controlled trophoblast invasion into uterine decidua is a critical process for the normal development of placenta, which is tightly regulated by various factors produced within the trophoblast-endometrial microenvironment. CXCL14 is involved in tumor growth and metastasis, and its expression in placenta is temporally regulated during pregnancy. However, the role of CXCL14 in trophoblast function during human pregnancy is not clear. In this study, by using RT-PCR through human pregnancy, we found that CXCL14 was selectively expressed at early but not late pregnancy. Immunostaining revealed that CXCL14 proteins were strongly expressed in villous cytotrophoblasts and moderately in decidualized stromal cells but very weakly in syncytiotrophoblasts and extravillous trophoblasts. The effect of CXCL14 on trophoblast invasion were examined by using human villous explants cultured on Matrigel and further proved by invasion and migration assay of primary trophoblast cells and trophoblast cell line HTR-8/SVneo. Our data showed that CXCL14 significantly inhibited outgrowth of villous explant in vitro; this effect is due to suppression of trophoblast invasion and migration through regulating matrix metalloproteinases activities, whereas the trophoblast proliferation was not affected. Moreover, because a receptor for CXCL14 has not been identified, we performed further cell-specific CXCL14 binding activities with regard to different cell types within the maternal-fetal interface. Our data revealed that CXCL14 could specifically bind to trophoblast cells but not decidual cells from the maternal-fetal interface. These results suggest that CXCL14 plays an important role in regulating trophoblast invasion through an autocrine/paracrine manner during early pregnancy.

150 IN VITRO MODEL FOR EFFECT OF ENDOCRINE-DISRUPTING CHEMICALS ON PLACENTAL CATION TRANSPORTER CHANNEL

2016 ◽  
Vol 28 (2) ◽  
pp. 205
Author(s):  
J.-H. Lee ◽  
M. H. Lee ◽  
M. J. Lee ◽  
E.-B. Jeung
Keyword(s):  
Cell Line ◽  
Steroid Hormones ◽  
Endocrine Disrupting Chemicals ◽  
Control Group ◽  
Bewo Cell ◽  
Mrna Levels ◽  
Phenol Red ◽  
Human Trophoblast ◽  
Protein Levels ◽  
Endocrine Disrupting

Calcium, copper, iron, oxygen, and carbon dioxide are essential factors in fetal growth. These molecules are transferred by specific receptors located on the cell membrane or cytoplasm in placenta. Calcium, copper, and iron transfer genes are regulated by oestrogen, placental lactogen, and vitamin D. During pregnancy, expression of these receptors is controlled by the nutritional status of the maternal and fetal environment. Some synthetic plastics contain endocrine-disrupting chemicals (EDC), which have similar structures to steroid hormones or endogenous hormones related to reproduction. These substances disturb action of hormones (e.g. increasing oestrogen or progesterone) by interacting with their receptors or affecting the expression of transporting genes for cations. We used a BeWo cell line (human trophoblast cell line) to test the effect of EDC during pregnancy. The cells were cultured in phenol red-free DMEM supplemented with 5% charcoal dextran-stripped fetal bovine serum for 48 h to ensure the depletion of steroid hormones in the cells. Ethinyl oestradiol (EE), which activates oestrogen receptors, was used as a positive control. Then, EE (10–9, 10–8, and 10–7 M), octylpehnol (OP; 10–7, 10–6, and 10–5 M), nonylphenol (NP; 10–8, 10–7, and 10–6 M), and bisphenol A (BPA; 10–7, 10–6, and 10–5 M) were treated in BeWo cells for 48 h, and the cells were harvested. The mRNA and protein levels for calcium transporting genes (PMCA1 and TRPV6), copper transporting genes (CTR1 and ATP7A), and iron transporting genes (IREG1 and HEPH) were quantified by RT-qPCR, and Western blotting, respectively. Experiments were carried 3 times, and results were statistically analysed by GraphPad Prism6 (GraphPad Software, San Diego, CA, USA). We observed dose-dependent decreases in mRNA levels of PMCA1, TRPV6, ATP7A, and IREG1 compared with control group in OP-, NP-, or BPA-treated groups. Protein levels showed a similar pattern to mRNA levels. Based on our data, we confirmed that these EDC affect metal ion channels such as calcium, copper, and iron transporters during pregnancy.

lncRNA deleted in lymphocytic leukaemia 1 (DLEU1) promotes the migration and invasion of human embryonic trophoblast cells

Zygote ◽  
2020 ◽  
Vol 28 (5) ◽  
pp. 397-402
Author(s):  
Zhongxiang Li ◽  
Mingbin Hou
Keyword(s):  
Small Interfering Rna ◽  
Lymphocytic Leukaemia ◽  
Quantitative Polymerase Chain Reaction ◽  
Regulatory Protein ◽  
Migration And Invasion ◽  
Control Group ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Interfering Rna ◽  
Human Trophoblast Cells

SummaryTo investigate the roles of lncRNA deleted in lymphocytic leukaemia 1 (DLEU1) on migration and invasion of human trophoblast cells. Human chorionic trophoblast cell line HTR8/SVneo was cultured and transfected using lncRNA DLEU1 small interfering RNA. Real-time quantitative polymerase chain reaction was used to detect lncRNA DLEU1 expression. The activity of migration regulatory protein CDC42 was detected by western blot. The downstream miRNA targets of lncRNA and mRNAs targeted by corresponding miRNAs were respectively predicted using bioinformatics analyses. Compared with the control group, the expression of lncRNA DLEU1 in the small interfering RNA group was significantly decreased (P < 0.05). There was no significant change in cell proliferation capacity for transfected cells (lncRNA DLEU1 siRNA-1, P = 0.537; lncRNA DLEU1 siRNA-2, P = 0.384), but cell migration (lncRNA DLEU1 siRNA-1, P = 0.025; lncRNA DLEU1 siRNA-2, P = 0.019) and invasion (lncRNA DLEU1 siRNA-1, P = 0.0327; lncRNA DLEU1 siRNA-2, P = 0.021) was significantly reduced. CDC42 activity in the lncRNA DLEU1 knockdown group decreased and the phosphorylation of cofilin increased. Therefore, downregulation of lncRNA DLEU1 suppressed the migration and invasion of human trophoblast cells.

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