6 research outputs found

    The effect of severity of pre-eclampsia on the basal plate intervillous surface lining components : a confocal laser scanning microscopy study

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    Financial support from Ghana government and GETFUND acknowledgedEThOS - Electronic Theses Online ServiceFinancial support from Ghana government and GETFUND acknowledgedGBUnited Kingdo

    The effect of severity of pre-eclampsia on the basal plate intervillous surface lining components: A confocal laser scanning microscopy study

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    Using immunofluoresce microscopy and histology, intervillous surface lining components area fractions were measured in healthy term chorionic plate (CP) (n=7), healthy term placental basal plate (n=11), mild pre-eclamptic (MPE) placental basal plate (n=10) and severe pre-eclamptic (SPE) placental basal plate (n=11). The aims are (1) to examine the effect of pre-eclampsia (PE) and its severity on the basal plate (BP) intervillous surface lining composition and (2) to define the composition of the CP intervillous surface lining. The results show the mean birth weight of the babies in the SPE are significantly lower than in the HC and MPE (F (2, 29) = 11.912, p =0.000) and the mean gestational age at delivery (GAD) in the SPE group is significantly lower than the HC and MPE (GAD) [Anova p = 0.001; posthoc, p =0.003 and p = 0.001 for MPE and healthy control (HC) respectively]. The mean anchoring villi (AV) to fibrin (NS) ratio of the BP intervillous surface lining is significantly lower in the SPE compared to MPE and the HC groups (ANOVA, p = 0.010; posthoc p = 0.009 and p = 0.628 for HC and MPE respectively) indicating increase fibrin deposition on the basal plate and decreasing anchoring villi attachment area with increasing severity of pre-eclampsia. There are no significant differences in the mean length fractions of endothelium and trophoblast between the 3 groups (Anova, p= 0.107 and p = 0.131 respectively). CP intervillous surface is lined partly by endothelium, trophoblast and an acellular material (fibrin/fibrinoid). Conclusions: (1) The inverse relationship between the proportions of fibrin and anchoring villi with increasing severity of pre-eclampsia indicates that increase deposition of the BP fibrin and poor trophoblast invasion of the BP underlies the disease progression. (2) The CP is partly endothelial contrary to the widely accepted view of wholly trophoblast

    Immunofluorescence confocal laser scanning microscopy and immuno-electron microscopic identification of keratins in human maternofetal interaction zone.

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    We show here that at least 5 keratin proteins are present in villous trophoblast and the same 5 in extravillous trophoblast. A further 14 tested were undetectable in these tissues. In contrast 10 of the 19 keratins tested were present in amniotic epithelium. The potential for marking amniotic epithelium on the one hand, as distinct from villous and extravillous trophoblast on the other can be achieved using 5 keratins (K4, 6, 13, 14 and 17) with a mixture of positive and negative discrimination that is expected, in combination, to be highly sensitive. All the specific keratins identified in trophoblast were apparently upregulated on the pathway to extravillous trophoblast. Co-ordinated differentiation at the molecular expression level is indicated by this finding. The relevant keratins are K5, 7, 8, 18 and19. Specific keratins have been identified that are down regulated in villous trophoblast in pre-eclamptic pregnancy. This difference between healthy and pre-eclamptic chorionic villous trophoblast keratin expression was statistically significant in 4 out of the 5 keratins. This was not the case for the extravillous trophoblast at the immunofluorescence confocal level but clear significant differences were obtained using immunogold electron microscopy. We suggest that the villous trophoblast in pre-eclamptic placentae is cytoskeletally weaker with respect to the filaments made from these specific proteins and that this is one reason why, in pre-eclampsia, trophoblast is deported in greater quantity than in healthy placentae

    Immuno-electron microscopic localisation of caveolin 1 in human placenta

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    We have localised the placental endothelial marker caveolin-1 at the ultrastructural level using indirect immunogold labelling. The particulate label has been quantified to assess the distribution of the target protein within term placental chorionic villi. The mesodermal compartment of the tissue was more heavily labelled than the ectodermally derived trophoblast. Basal plate lining endothelium, and villous endothelium had similar immunoreactivity with anti-caveolin-1 antibody. A polarised distribution of the caveolin within chorionic villous capillary endothelial cells was observed. As evidenced by immuno-reactivity, the protein was statistically significantly more concentrated in the region associated with the basal membrane than the apical membrane. The latter region contained in turn significantly more anticaveolin-1 immunoreactivity than the central region. These differences are discussed in the light of possible transport and signalling platform roles for villous and basal plate endothelium. (c) 2006 Elsevier GmbH. All rights reserved
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