Phenotype of the endothelium in the human term placenta
ABSTRACT The placental endothelium contributes to regulating transplacental exchange and maintaining the immunological maternofetal barrier. We characterized the endothelial phenotype in human normal term placentae with a panel of antibodies to endothelial antigens using a standardized immunofluorescence method. Placental endothelium strongly expressed vWF, PAL-E, H-antigen, thrombomodulin, PECAM-1, CD34, CD36, ICAM-1, CD44, thy-1, A10/33-1, VE-cadherin, caveolin-1 and HLA-G, whereas occludin, claudin-1, eNOS, angiotensin converting enzyme (ACE), ICAM-2, endoglin and integrin-alphathetabeta(3)were weakly expressed. PGI(2)synthase, tissue factor, E-selectin and VCAM-1 were not detected. Some antigens were heterogenously expressed along the vascular tree or within individual villi. Expression of ACE, eNOS, vWF, P-selectin, E-selectin, integrin alpha(v)beta(3)and endoglin was stronger in the maternal decidual vessels, while PECAM-1, CD44, thy-1 and caveolin-1 expression was stronger in fetal vessels. Some endothelial markers were present in trophoblasts and stroma. Endothelial proliferation was apparent in mature intermediate and terminal villi. There was limited inflammatory response to TNFalpha in explants, characterized by upregulation of vWF, P-selectin, PECAM-1 and CD44, downregulation of thrombomodulin, but no increase in ICAM-1 expression, nor induction of E-selectin, VCAM-1 or tissue factor. These patterns of heterogeneity, proliferative activity and inflammatory activation may underlie the specific physiological roles of the placental endothelium.
- SourceAvailable from: John M. Brameld
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- "Angiotensin converting enzyme (ACE) cleaves the C-terminal dipeptide from angiotensin I to form AngII. ACE was identified in the placenta more than 30 years ago. It is more weakly expressed in placental than in decidual vascular endothelium ; if it is ratelimiting in the generation of AngII in feto-placental vessels, changes in activity could be of functional significance. We hypothesized that ACE activity in the chorionic plate arteries would increase to the periphery, and that ACE activity would relate to placental or birthweight. "
ABSTRACT: Sensitivity of chorionic plate arteries to angiotensin II (AngII) is greatest at the placental periphery. Angiotensin converting enzyme (ACE) is central to the synthesis of AngII and is present in the placental vasculature. We measured vascular ACE activity/mg protein at 8-9 sites between the cord insertion and the periphery in 12 term placentae from normotensive, vaginally-delivered women. ACE increased from insertion to the periphery (P = 0.015); median ACE for each placenta was positively correlated with placental weight (P < 0.05) and placental:birthweight ratio (P < 0.02). We speculate that this may be related to fetal programming since placental:birthweight ratio is related to long-term health.Placenta 08/2011; 32(11):906-8. DOI:10.1016/j.placenta.2011.07.085 · 3.29 Impact Factor
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- "We characterised the phenotypes of the cells in the region using indirect confocal immunofluorescence microscopy and isotype controls for the monoclonal first step antibodies. Our methods yielded results consistent with those of others    when applied to components of the neighbouring chorionic villous tree (syncytiotrophoblast and fetal capillary endothelium in the mesenchymal cores of tertiary villi). When applied in single and dual labelling studies to the basal plate lining some parts showed immunofluorescence characteristic of trophoblast but not endothelium and other parts immunofluorescence characteristic of endothelium but not trophoblast. "
ABSTRACT: An unusual monolayer of cells lines the interface between the basal plate and the intervillous space in human term placenta but not the chorionic villi. Our recent descriptions of it are based on advanced microscopy, phenotyping and cytogenetic approaches. The papers show that the layer is partly epithelial (ectoderm) and partly endothelial (mesoderm): it is partly derived from the fetus and partly from the mother. This first accurate description of a naturally occurring human allo-epi-endothelium (monolayer of cells derived from two embryological germ layers and two individuals) is of interest in anatomy, obstetrics and gynaecology, developmental biology, histology and immunology. The most extensive evidence for this mosaic applies to the intervillous space lining layer of the basal plate where the endothelial proportion is of the order of 50%; it extends throughout central, intermediate and peripheral parts of the basal plate and is a consistent feature of the intervillous space lining of the chorionic plate also. Its presence lining chorionic plate is noteworthy as it includes the furthest parts of the sinus from the supplying and draining vessels which are endothelial lined.Placenta 10/2010; 31(12):1035-42. DOI:10.1016/j.placenta.2010.09.007 · 3.29 Impact Factor
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- "To assess whether the decreased level of the CCN molecules in early pre-eclamptic placentae was because of a lower proportion of endothelial cells in the chorionic villi tissue—the cell type where CYR61 and NOV were strongly coexpressed—we evaluated the mRNA expression level of the vascular endothelial cell marker CD34. The transmembrane protein CD34 is a reliable and well-accepted marker for the endothelium which is, in the placenta, only expressed in fetal and maternal vessels but not in the trophoblast (Dye et al., 2001; Huppertz, 2006), whereas the endothelial marker CD31 was also found to be expressed in subpopulations of trophoblast cells as well as on platelets, monocytes and lymphocytes and thus not suitable for western blot analysis (Coukos et al., 1998; Dye et al., 2001). Realtime PCR analysis revealed a significant up-regulation of CD34 in early pre-eclamptic placentae compared with normal matched controls , suggesting that either the amount of endothelial cells or the CD34 expression level per cell was elevated (Figure 4C). "
ABSTRACT: The pregnancy disorder pre-eclampsia (PE) is thought to be caused in part by shallow invasion of the extravillous trophoblast (EVT) leading to uteroplacental insufficiency and hypoxia. Here, we focused on the expressions of cysteine-rich 61 (CYR61, CCN1) and nephroblastoma overexpressed (NOV, CCN3), members of the CCN family of angiogenic regulators, in human placenta during normal pregnancy compared with pre-eclamptic and HELLP placentae using quantitative RT-PCR, western blotting and immunocytochemistry. During normal pregnancy, both proteins showed increasing expression levels and were strongly coexpressed in endothelial cells of vessels, stromal cells and interstitial EVT giant cells. However, NOV showed an earlier onset of expression in villous endothelial cells during gestation compared with CYR61, which may signify distinct roles of these proteins in placental angiogenesis. In early-onset pre-eclamptic placentae, both CYR61 and NOV were expressed at a significantly lower level compared with normal matched controls. This decrease of CYR61 and NOV in pre-eclamptic placentae is not associated with a decrease of the endothelial marker CD34 or vimentin. No obvious changes in the localization of CYR61 and NOV in pre-eclamptic placentae were detected but a change in the intracellular distribution in trophoblast giant cells. Our data point to a potential role of both molecules in the pathogenesis of early-onset PE.Molecular Human Reproduction 07/2006; 12(6):389-99. DOI:10.1093/molehr/gal044 · 3.48 Impact Factor