References of "Placenta"
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See detailIFPA Meeting 2012 Workshop Report III: trophoblast deportation, gestational trophoblastic disease, placental insufficiency and fetal growth restriction, trophoblast over-invasion and accreta-related pathologies, placental thrombosis and fibrinolysis.
Al-Khan, A.; Bulmer, J. N.; CHANTRAINE, Frédéric ULg et al

in Placenta (2013), 34 Suppl

Workshops are an important part of the IFPA annual meeting as they allow for discussion of specialized topics. At IFPA meeting 2012 there were twelve themed workshops, five of which are summarized in this ... [more ▼]

Workshops are an important part of the IFPA annual meeting as they allow for discussion of specialized topics. At IFPA meeting 2012 there were twelve themed workshops, five of which are summarized in this report. These workshops related to various aspects of placental biology but collectively covered areas of clinical research and pregnancy disorders: 1) trophoblast deportation; 2) gestational trophoblastic disease; 3) placental insufficiency and fetal growth restriction; 4) trophoblast overinvasion and accreta-related pathologies; 5) placental thrombosis and fibrinolysis. [less ▲]

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See detailTGFbeta-receptor-dependent angiostimulation through the hyperglycosylated isoform of human chorionic gonadotropin.
Berndt, Sarah; Detilleux, Julien; Blacher, Silvia et al

in Placenta (2011), 32(9), 44

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See detailFetal growth restriction: a workshop report
Cetin, I.; Foidart, Jean-Michel ULg; Miozzo, M. et al

in Placenta (2004), 25(8-9), 753-757

Intrauterine growth restriction (IUGR) is associated with significantly increased perinatal morbidity and mortality as well as cardiovascular disease and glucose intolerance in adult life. A number of ... [more ▼]

Intrauterine growth restriction (IUGR) is associated with significantly increased perinatal morbidity and mortality as well as cardiovascular disease and glucose intolerance in adult life. A number of disorders from genetic to metabolic, vascular, coagulative, autoimmune, as well as infectious, can influence fetal growth by damaging the placenta, leading to IUGR as a result of many possible fetal, placental and maternal disorders. Strict definitions of IUGR and of its severity are needed in order to eventually distinguish among different phenotypes, such as gestational age at onset, degree of growth restriction and presence of hypoxia. This report explores and reviews some of the most recent developments in both clinical and basic research on intrauterine growth restriction, by seeking mechanisms that involve genetic factors, utero-placental nutrient availability and vascular growth factors. New exciting findings on the genomic imprinting defects potentially associated with IUGR, and the placental anomalies associated with the decreased nutrient transport are summarized. Moreover, recent data on angiogenic growth factors as well as new information arising from application of gene chip technologies are discussed. (C) 2004 Elsevier Ltd. All rights reserved. [less ▲]

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See detailDemonstration of the expression of CD95 ligand transcript and protein in human placenta
Zorzi, Willy ULg; Thellin, Olivier ULg; Coumans, Bernard ULg et al

in Placenta (1998), 19(4), 269-277

Tolerance of the fetal allograft enables the human conceptus to implant itself into the maternal uterus and survive and grow there. This tolerance phenomenon remains largely obscure, notably because it ... [more ▼]

Tolerance of the fetal allograft enables the human conceptus to implant itself into the maternal uterus and survive and grow there. This tolerance phenomenon remains largely obscure, notably because it appears to be controlled by multiple mechanisms. CD95 ligand (CD95-L), which can trigger death of CD95-positive cells by apoptosis, may participate in inducing anti-fetus-sensitized CD95-positive T lymphocytes to enter apoptosis. Using immunohistochemistry (first trimester and term placentae), FAGS assays (term placenta) and RT-PCR assays (term placenta), the presence of CD95-L protein and mRNA has been shown in crude placental tissue preparations and isolated placental cells. Among the latter, CD95-L expression was detected in trophoblastic cells, fetal blood cells (mRNA only) and also the Hofbauer macrophages. No CD95-L was detected in fibroblasts or fetal endothelial cells. Thus trophoblastic cells, Hofbauer macrophages, and perhaps also fetal blood cells could form a sequential barrier blocking maternal activated defence cells bearing CD95 molecules. (C) 1998 W. B. Saunders Company Ltd. [less ▲]

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See detailExpression of Stromelysin-3 in the Human Placenta and Placental Bed
Maquoi, Erik ULg; Polette, M.; Nawrocki, B. et al

in Placenta (1997), 18(4), 277-85

Human placentation is mediated by fetal trophoblastic cells which penetrate into the decidualized uterine endometrium. Trophoblast invasion requires the precisely regulated secretion of specific ... [more ▼]

Human placentation is mediated by fetal trophoblastic cells which penetrate into the decidualized uterine endometrium. Trophoblast invasion requires the precisely regulated secretion of specific proteinases able to degrade the endometrial basement membranes and extracellular matrix. To document further the involvement of these proteinases during human placentation, we evaluated in vivo the expression of stromelysin-3, a member of the metalloproteinase family, during the first and third trimesters of pregnancy, by means of immunohistochemistry, in situ hybridization and Northern blot analysis. Human extravillous trophoblasts invading the maternal decidua produced stromelysin-3 during both, the first and third trimesters of pregnancy, but to a lesser extent during the latter. In floating villi, stromelysin-3 expression was restricted to the syncytiotrophoblasts that line intervillous vascular spaces. In conclusion, stromelysin-3 is expressed by differentiated, non-proliferative villous and extravillous trophoblastic cells in early and late placental beds and villi, and its pattern of expression evolves during pregnancy. Our observations suggest that stromelysin-3 could play a role in human placentation. [less ▲]

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See detailChanges in the Distribution Pattern of Galectin-1 and Galectin-3 in Human Placenta Correlates with the Differentiation Pathways of Trophoblasts
Maquoi, Erik ULg; van den Brule, F. A.; Castronovo, Vincenzo ULg et al

in Placenta (1997), 18(5-6, Jul-Aug), 433-9

Human placentation is a complex biological phenomenon that results from precisely regulated interactions between cells and the extracellular matrix. Galectin- 1 and galectin-3 belong to a newly defined ... [more ▼]

Human placentation is a complex biological phenomenon that results from precisely regulated interactions between cells and the extracellular matrix. Galectin- 1 and galectin-3 belong to a newly defined family of galactose-binding lectins that can bind several glycoconjugates such as the basement membrane glycoprotein laminin, and are involved in many biological events including cell adhesion. In this study, the expression of these two galectins in first and third trimester normal human placenta was examined using single and double immunohistochemical staining and specific antibodies for galectins and cytokeratins. Galectin-3 was detected in all trophoblastic lineages including villous cytotrophoblasts and extravillous trophoblasts (trophoblastic cell columns, infiltrating trophoblasts, endovascular trophoblasts and placental bed giant cells). On the contrary, galectin-1 distribution was restricted to endometrium. A reduction of galectin-3 expression was observed from the villous trophoblasts to the trophoblastic cell columns. This pattern correlated with the switch from a proliferative to a migratory phenotype. Galectin-1 and galectin-3 were both detected in maternal decidual cells. Our data demonstrate a specific pattern of galectin-1 and galectin-3 expression in trophoblastic tissue, and suggest these lectins could contribute to cell-cell and cell matrix interactions of trophoblast during placentation. [less ▲]

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See detailMembrane-type matrix metalloproteinase-1 expression at the site of human placentation
Nawrocki, B.; Polette, M. E.; Marchand, V. et al

in Placenta (1996), 17(8), 565-72

Human trophoblast implantation is a highly regulated process of invasion that requires action of proteolytic enzymes to degrade extracellular matrix components of the endometrium. Among these enzymes ... [more ▼]

Human trophoblast implantation is a highly regulated process of invasion that requires action of proteolytic enzymes to degrade extracellular matrix components of the endometrium. Among these enzymes, matrix metalloproteinases (MMPs) seem to be particularly important in this degradative process. We previously showed that gelatinase A is extensively expressed in vivo in the human placenta. A new MMP, MT-MMP-1 (membrane-type matrix metalloproteinase-1), which is thought to activate progelatinase A, has recently been described. In this study, we examined the expression of MT-MMP-1, by immunohistochemistry and in situ hybridization, in human placental bed biopsies taken during the first trimester of gestation. Human first trimester intermediate trophoblasts synthesized MT-MMP-1 mRNAs and the protein. The MT-MMP-1 pattern of distribution in placental beds was similar to that of gelatinase A, suggesting a pivotal role for MT-MMP-1 in placentation, perhaps by activating progelatinase A. [less ▲]

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See detailGalactose Alpha 1-3 Galactose and Anti-Alpha Galactose Antibody in Normal and Pathological Pregnancies
Christiane, Y.; Aghayan, M.; Emonard, H. et al

in Placenta (1992), 13(5, Sep-Oct), 475-87

The galactose alpha 1-3 galactose (Gal alpha 1-3 Gal) residue is a carbohydrate widely distributed in many non-human mammals. Since Gal alpha 1-3 Gal residues are described on the cell surface of tumor ... [more ▼]

The galactose alpha 1-3 galactose (Gal alpha 1-3 Gal) residue is a carbohydrate widely distributed in many non-human mammals. Since Gal alpha 1-3 Gal residues are described on the cell surface of tumor cells, we have examined the possibility of their expression on human trophoblastic cells at different stages of placental implantation and in various pregnancy-associated conditions. Using immunohistochemical methods, Gal alpha 1-3 Gal was demonstrated on interstitial and vascular trophoblast during pregnancy. For villous trophoblast, the staining disappeared in second trimester pregnancies. The density of staining for Gal alpha 1-3 Gal was increased in highly invasive trophoblast (mole and choriocarcinoma) and decreased in poorly invasive specimens (spontaneous abortion, XO monosomia). No cells displaying Gal alpha 1-3 Gal at their surface were identified in some segments of spiral arteries from pre-eclamptic women. The anti-Gal antibody titer increased in the first trimester of pregnancy and in the sera of pre-eclamptic and eclamptic patients. These findings suggest that Gal alpha 1-3 Gal residues could be considered as markers for trophoblast invasive capacity and that the binding of maternal anti-Gal antibodies to the trophoblast could contribute to limit trophoblastic invasion and thus participate to the immunological control of implantation. [less ▲]

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See detailThe basement membrane proteins laminin and type IV collagen in isolated villi in pre-eclampsia
Risteli, J.; Foidart, Jean-Michel ULg; Risteli, L. et al

in Placenta (1984), 5(6), 541-50

The distribution and concentrations of the basement membrane proteins laminin and type IV collagen were studied in isolated placental villi in normal pregnancy and in pre-eclampsia. In both cases these ... [more ▼]

The distribution and concentrations of the basement membrane proteins laminin and type IV collagen were studied in isolated placental villi in normal pregnancy and in pre-eclampsia. In both cases these proteins could be localized by immunofluorescence in the trophoblast and capillary basement membranes, and occasionally also in the matrix surrounding the capillaries. The basement membrane proteins were quantified by solubilizing the villi with proteolytic enzymes and by subsequently measuring the concentrations of two resistant domains of these proteins (7-S collagen and the fragment PI, representing type IV collagen and laminin, respectively) with specific radioimmunoassays. The ratio type IV collagen:laminin was significantly higher in pre-eclamptic samples than in the controls, most probably reflecting a decrease in laminin concentration in the villi in pre-eclampsia. Such a change in the chemical composition of placental basement membranes could weaken the attachment of trophoblast cells to the underlying basement membrane and also modify the permeability and exchange properties of the villi. [less ▲]

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See detailMaternal vascular lesions in pre-eclampsia and intrauterine growth retardation: light microscopy and immunofluorescence.
Hustin, J.; Foidart, Jean-Michel ULg; Lambotte, R.

in Placenta (1983), 4

Placental bed biopsies were performed during caesarean section in a series of 137 patients. Analysis of the morphological findings confirms that vascular physiological changes were reduced in pre ... [more ▼]

Placental bed biopsies were performed during caesarean section in a series of 137 patients. Analysis of the morphological findings confirms that vascular physiological changes were reduced in pre-eclampsia and in normotensive intrauterine growth retardation. In pre-eclampsia, acute atherosis in the decidual segments of uteroplacental arteries was a prominent feature. Intimal thickenings of the myometrial segments of the uteromaternal arteries were also noted. Normotensive intrauterine growth retardation cases were characterized by intimal thickenings of the myometrial segments of the uteroplacental arteries. Immunofluorescent investigations have demonstrated that the deep vascular stenoses were not associated with immunoglobulin deposition while in distal arterial segments displaying acute atherosis a positive immunofluorescence for IgG and fibrin and, more irregularly, for C'3 and IgM could be noted. These findings lead us to suggest that an immunological mechanism may be involved in the pathogenesis of acute atherosis. [less ▲]

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