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Syncytiotrophoblast Cells (syncytiotrophoblast + cell)
Selected AbstractsPlacental macrophage contact induces complete replicative cycle of human immunodeficiency virus in latently infected syncytiotrophoblast cells: role of interleukine-6 and tumor necrosis factor-,AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2002Ferenc D. Tóth The phenotypic mixing between human immunodeficiency virus type 1 (HIV-1) and vesicular stomatitis virus (VSV) has been exploited to assay the susceptibility of human term syncytiotrophoblast cells to penetration by various strains of HIV-1. VSV (HIV-1IIIB) and VSV (HIV-1Ba-L) pseudotypes were found to enter syncytiotrophoblasts. Infection of syncytiotrophoblasts was mediated by envelope glycoproteins of IIIB and Ba-L strains of HIV-1. Although certain strains of HIV-1 could enter syncytiotrophoblasts, the cells did not exhibit permissiveness for HIV-1. The next studies tested the possibility that placental macrophages might induce replication of HIV-1 carried in syncytiotrophoblast cells and that infected syncytiotrophoblasts would be capable of transmitting virus into neighbouring macrophages. For this purpose, the macrophage-tropic Ba-L strain of HIV-1 was used. Interactions between syncytiotrophoblasts and macrophages activated HIV-1 from latency in syncytiotrophoblast cells, which delivered HIV-1 to cocultured macrophages. The stimulatory effect of coculture on HIV-1 gene expression was mediated by marked tumor necrosis factor-, and interleukin-6 release from macrophages, an effect caused by contact between the different placental cells. Results suggest an interactive role for the syncytiotrophoblast layer and placental macrophages in the dissemination of HIV-1 among placental tissue. [source] Placental endothelial nitric oxide synthase localization and expression in normal human pregnancy and pre-eclampsiaCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2003SJ Orange Summary 1.,The aim of the present study was to investigate whether pre-eclampisa, a state of placental hypoxia, is associated with placental abnormalities in the amount, distribution and expression of enothelial nitric oxide synthase (eNOS). 2.,Localization and intensity of eNOS was determined by immunohistochemistry using an antibody specific for eNOS. The amount of eNOS mRNA expression was determined by reverse transcription,polymerase chain reaction (RT-PCR) and the densitometry of gel bands was expressed as a ratio of the band density of the housekeeping gene ,2 -microglobulin. 3.,Endothelial NOS staining was localized to syncytiotrophoblast cells within the villi and decidual trophoblast cells. It was not present in the endothelium of terminal villous vessels. There was no significant difference in eNOS villous or decidual staining intensity between normal pregnancy (NP; n = 12), pre-eclampsia (n = 14), or gestational hypertension (GH; n = 4). Staining for eNOS was not significantly different in the decidua compared with the villi in NP, GH or pre-eclampsia. Within the decidua, the depth of eNOS staining was similar in NP, pre-eclampisa and GH. 4.,There was no significant difference in eNOS mRNA expression between NP (0.70 ± 0.11), pre-eclampsia (0.5 ± 0.07) or GH (0.69 ± 0.26). 5.,These findings suggest that the amount of eNOS in the placenta is not deficient in pre-eclampsia, excluding a possible pathogenic role for eNOS in this disease. Furthermore, placental hypoxia, which is associated with pre-eclampsia, did not induce an upregulation of eNOS [source] | ||||||||||