Endometrial secretions: creating a stimulatory microenvironment within the human early placenta and implications for the aetiopathogenesis of preeclampsia

2011 ◽  
Vol 89 (2) ◽  
pp. 118-125 ◽  
Author(s):  
G.J. Burton ◽  
M. Scioscia ◽  
T.W. Rademacher
Keyword(s):  
Retrovirology ◽  
2009 ◽  
Vol 6 (Suppl 1) ◽  
pp. O2
Author(s):  
Benjamin Rauwel ◽  
Bernard Mariamé ◽  
Hélène Martin ◽  
Danièle Evain-Brion ◽  
Thierry Fournier ◽  
...  
Keyword(s):  
De Novo ◽  

Development ◽  
2001 ◽  
Vol 128 (6) ◽  
pp. 827-838 ◽  
Author(s):  
B. Isermann ◽  
S.B. Hendrickson ◽  
K. Hutley ◽  
M. Wing ◽  
H. Weiler

The endothelial cell surface receptor thrombomodulin (TM) inhibits blood coagulation by forming a complex with thrombin, which then converts protein C into the natural anticoagulant, activated protein C. In mice, a loss of TM function causes embryonic lethality at day 8.5 p.c. (post coitum) before establishment of a functional cardiovascular system. At this developmental stage, TM is expressed in the developing vasculature of the embryo proper, as well as in non-endothelial cells of the early placenta, giant trophoblast and parietal endoderm. Here, we show that reconstitution of TM expression in extraembryonic tissue by aggregation of tetraploid wild-type embryos with TM-null embryonic stem cells rescues TM-null embryos from early lethality. TM-null tetraploid embryos develop normally during midgestation, but encounter a secondary developmental block between days 12.5 and 16.5 p.c. Embryos lacking TM develop lethal consumptive coagulopathy during this period, and no live embryos are retrieved at term. Morphogenesis of embryonic blood vessels and other organs appears normal before E15. These findings demonstrate a dual role of TM in development, and that a loss of TM function disrupts mouse embryogenesis at two different stages. These two functions of TM are exerted in two distinct tissues: expression of TM in non-endothelial extraembryonic tissues is required for proper function of the early placenta, while the absence of TM from embryonic blood vessel endothelium causes lethal consumptive coagulopathy.


2015 ◽  
Vol 04 (04) ◽  
pp. 190-194
Author(s):  
Khan Mohd Anas ◽  
Sinha D N. ◽  
Singh AK ◽  
Deopa Deepa ◽  
Niranjan Richa

Abstract Background : Placenta along with its umbilical cord is a vital organ for maintaining pregnancy and promoting normal foetal development. Foetal outcome can be adversely influenced by pathological changes in placenta and also by the variation in the site of attachment of umbilical cord. Aims and Objectives : To study the incidence of furcate umbilical cord insertion over placental chorionic plate in normal full term pregnancy. Materials and methods : This study was conducted in the department of Anatomy Government Medical College Haldwani. 100 freshly delivered placentae were collected from Dr. Sushila Tiwari Government hospital Haldwani. The sample was further categorized according to the parity of mother into two groups primipara (n=39) and multipara (n=61). Placentae included in the study were obtained from full term pregnancy without any complication like diabetes, hypertension etc. Results : The incidence of furcate umbilical cord in the present study was 2.6% in primipara group and 3.3% in multipara group. Conclusion : Variation in the site of insertion of umbilical cord are thought to result from process known as "Trophotropism" in which the chorionic frondosum or the early placenta migrates with advancing gestation to ensure better blood supply from more richly vascularised area. The overall incidence of furcate cord in this study is 3%. We have noticed one furcate cord (2.6%) in primipara group (n=39) and two furcate cords (3.3%) in multipara group (n=61). The neonates delivered were perfectly healthy without any evidence of congenital anomalies.


Placenta ◽  
1982 ◽  
Vol 3 (2) ◽  
pp. 197-209 ◽  
Author(s):  
S. Żonierowicz ◽  
J. Świerczyński ◽  
L. Żelewski

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 20069-20069
Author(s):  
J. Ayllon ◽  
S. Oudard ◽  
E. Banu ◽  
J. L. Janneau ◽  
D. Helley ◽  
...  

20069 Background: Some studies suggest a causal relationship between the early placenta insuline-like peptide encoded by the insulin-like 4 gene and cancer invasiveness. Methods: Serum concentrations of pro-EPIL were measured by ELISA using a novel two-site “sandwitch” assay, based on two monoclonal antibodies (mAb) raised against synthetic peptides analogous to two distinct regions of the pro-Epil polypeptide: mAb EPIL15, and biotinylated mAb EPIL02, used as the labelled indicator. The first mAb EPIL15 was purified and bound to a solid phase. Pro-EPIL was allowed to bind, and unbound proteins were removed by washing. The sensitivity limit of the assay was 3 ng/mL of synthetic peptide, and detection was linear over a range of at 3 pg to 200 ng of the synthetic peptide. As primary endpoint, we studied the Pro-EPIL distribution according to some clinico-biological prognostic factors. Results: Between July 2001 and April 2005, nineteen chemonaive NSCLC pts were treated by chemotherapy in our center and serum determinations of pro-EPIL were performed. Ten pts (63%) overexpressed pro-EPIL before start of chemotherapy with a median value of 1.06 ng/mL (range 0.01–6.75). Median age was 60 years (range 38–80), more than 90% of pts were men with an advanced or metastatic disease. Forty-two percent of pts had a large cell carcinoma subtype, with 25% of adenocarcinoma and 25% of epidermoid type. Immunologic evaluations were performed with a median value of the CD3+ lymphocites of 1290/mm3 (range 610–2138). Significant correlations were observed between age, serum alcaline phosphatase and CD3+ number. A border-line positive correlation was observed between pro-EPIL and CD3+ levels (P = 0.09, R2 = 0.5). Median OS for entire cohort was 7.5 months (95% CI, 5.5–9.4), with 67% deaths. Because our sample size was very low, no survival analysis were performed according to the baseline pro-EPIL value and other prognostic factors. A bootstrapping procedure is planned on our data. Conclusions: This results showed that pro-EPIL was overexpressed in the majority of advanced NSCLC pts. Interactions between this biomarker and immune system are possible. Furthemore, pro-EPIL as a therapeutic target might be tested in prospective studies. No significant financial relationships to disclose.


2021 ◽  
Author(s):  
Hirosuke Shiura ◽  
Ryuichi Ono ◽  
Saori Tachibana ◽  
Takashi Kohda ◽  
Tomoko Kaneko-Ishino ◽  
...  

AbstractThe therian-specific gene paternally expressed 10 (Peg10) plays an essential role in placenta formation: Peg10 knockout (KO) mice exhibit early embryonic lethality due to severe placental defects. The PEG10 protein exhibits homology to long terminal repeat (LTR) retrotransposon GAG and POL proteins, therefore mice harboring a mutation in its highly conserved viral aspartic protease motif in the POL-like region were generated because it is essential for LTR retrotransposons/retroviruses. Intriguingly, frequent perinatal lethality, not early embryonic lethality, was observed with fetal and placental growth retardation starting mid-gestation. In the mutant placentas, severe defects were observed in the fetal vasculature, where PEG10 is expressed in the three trophoblast cell layers that surround fetal capillary endothelial cells. Thus, Peg10 has essential roles not only in early placenta formation, but also in placental vasculature maintenance from mid- to late-gestation. This implies that along the feto-maternal placenta interface an interaction occurs between two retrovirus-derived genes, Peg10 and retrotransposon Gag like 1 (Rtl1, also called Peg11), that is essential for the maintenance of fetal capillary endothelial cells.Summary statementDisruption of the highly conserved viral aspartic protease domain in PEG10 causes placental abnormality leading to perinatal lethality in mice.


2021 ◽  
Vol 7 (33) ◽  
pp. eabf4416
Author(s):  
Yanxing Wei ◽  
Tianyu Wang ◽  
Lishi Ma ◽  
Yanqi Zhang ◽  
Yuan Zhao ◽  
...  

Human trophoblast stem cells (hTSCs) provide a valuable model to study placental development and function. While primary hTSCs have been derived from embryos/early placenta, and transdifferentiated hTSCs from naïve human pluripotent stem cells (hPSCs), the generation of hTSCs from primed PSCs is problematic. We report the successful generation of TSCs from primed hPSCs and show that BMP4 substantially enhances this process. TSCs derived from primed hPSCs are similar to blastocyst-derived hTSCs in terms of morphology, proliferation, differentiation potential, and gene expression. We define the chromatin accessibility dynamics and histone modifications (H3K4me3/H3K27me3) that specify hPSC-derived TSCs. Consistent with low density of H3K27me3 in primed hPSC-derived hTSCs, we show that knockout of H3K27 methyltransferases (EZH1/2) increases the efficiency of hTSC derivation from primed hPSCs. Efficient derivation of hTSCs from primed hPSCs provides a simple and powerful model to understand human trophoblast development, including the pathogenesis of trophoblast-related disorders, by generating disease-specific hTSCs.


BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Philip Savage ◽  
David Monk ◽  
Jose R. Hernandez Mora ◽  
Nick van der Westhuizen ◽  
Jennifer Rauw ◽  
...  

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