PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11978068

In vitro models to study trophoblast function and dysfunction-- a workshop report.

D W Morrish·G St J Whitley·J E Cartwright·C H Graham·I Caniggia
View original source ↗Export metadata ↓

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Chorionic VilliCoculture TechniquesFemaleFetal HypoxiaGestational AgeHumansModels, BiologicalPregnancyTrophoblastsConference Proceedings

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D W Morrish, G St J Whitley, J E Cartwright, C H Graham, I Caniggia. 2002. In vitro models to study trophoblast function and dysfunction-- a workshop report.. https://doi.org/10.1053/plac.2002.0798

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Prenatal diagnosis in hemophilia A using factor VIII gene polymorphism--Indian experience.

The heterogeneous nature of the mutations, the size, and the complexity of the factor VIII gene makes direct mutation analysis in hemophilia A families in India an option that is not very feasible and practical. Thus, carrier screening and prenatal diagnosis of hemophilia A often depends on haplotype analysis using restriction fragment length polymorphisms (RFLP) and short tandem repeat (STR) markers to track the defective factor VIII gene within a family. The main objective of this present study was to assess the utility of using polymerase chain reaction (PCR)-based five polymorphic markers: four intragenic Hind III, Bcl I, intron 13, and intron 22 STRs and one extragenic marker St14 in prenatal diagnosis. Forty-one chorionic villus samples (CVS) were studied from 41 families with a history of hemophilia A. PCR and RFLP were used for screening. Intron 22 STR showed the highest informativeness (60.9%), followed by Hind III (51.2%), Bcl I (46.3%), & intron 13 STR (51.2%); the extragenic marker St14 (VNTR) was informative in 46.3% of families. Linkage analysis, with the combined use of these five PCR-based polymorphic markers, gives good informativeness of 87.8% in the Indian population. Of the 41 CVS tested, 21 were found to be male fetuses and of these 13 were found likely to be affected with hemophilia A. Only in 12.2% of the families were none of the markers informative.

Chorionic Villi↗
PubMed2003

[Villitis of unknown etiology in placentas of pregnancies with hypertensive disorders and of small-for-gestational-age infants].

BACKGROUND: The objectives of this study are to analyze the frequency and the histopathological features of the villitis of unknown etiology (VUE) in placentas of pregnancies with hypertensive disorders and of small-for-gestational-age infants (SGA). METHODS: Two hundred and thirteen placentas from pregnancies without clinical or laboratorial evidence of infection were studied. These cases were subdivided according to: a) maternal condition in: non-complicated pregnancy (NCP)- 151 cases, pregnancy-induced hypertension (PIH)- 37 and sustained chronic hypertension (SCH)- 25 and b) newborn weight in: small for gestational age (SGA)- 38 cases and adequate for gestational age (AGA)- 175. Of these placentas, 81 belong to the random sample, which was used to determine the frequency of VUE in the population studied. Eight blocks were taken from placental parenchyma and the histological sections were stained with hematoxylin and eosin. Frequency tables of categorical data were analyzed using the chi- square test and Fisher test; statistical significance was considered for p< 0.05. RESULTS: The frequency of VUE in the placentas was 30.8% in the random sample, 39% in NCP, 29.7% in PIH, 32% in SCH, 34.2% in SGA infants and 37.1% in AGA infants. Placentas of pregnancies with hypertensive disorders were more affected by villitis with parenchymatous component (PIH - 27.0%, SCH - 28.0%). This lesion was also the predominant villitis in the placentas of the SGA infants (31.5%). In contrast, in placentas of NCP and AGA infants, the principal kind of villitis was basal, not associated to a parenchymatous component (16.5% and 14.8% respectively). In the majority of the cases the villitis was mild. CONCLUSION: In the population studied, the frequency of VUE is high (around 30%). The lesion occurs in a similar frequency in placentas from NCP, PIH, SCH, SGA and AGA infants, but basal villitis not associated to a parenchymatous component affects mainly the placentas of NCP and AGA infants. It is possible that this kind of villitis could be an expression of an antigenic stimulation diverse from villitis with a parenchymatous component.

Chorionic Villi↗
PubMed2003

The pattern of expression of protease-activated receptors (PARs) during early trophoblast development.

Human fetal development depends on the ability of the embryo to gain access to the maternal circulation. Thus, specialized stem cells of the newly formed placenta, trophoblast, invade the uterus and its arterial network to establish an efficient feto-maternal molecular exchange. To accomplish this task, trophoblast differentiation during the first trimester of pregnancy involves cell proliferation, invasion, and extracellular matrix (ECM) remodelling. Trophoblast invasion shares many features with tumour cell invasion, with the distinction that it is strictly spatially and temporally controlled. We have previously demonstrated that PAR1, the first member of the protease-activated receptor (PAR) family, plays a central role in tumour cell invasion. In the present study we have examined the pattern of expression of PAR1 and other PAR family candidates during early human placental development. We show that PAR1 and PAR3 are highly and spatially expressed between the 7th and 10th weeks of gestation but not at the 12th week and thereafter. Likewise, high expression levels of PAR1 and PAR3 were observed in the cytotrophoblast cells of complete hydatidiform mole as compared to minimal levels in normal age-matched placenta. Together, our data suggest the involvement of PAR1 and PAR3 in restricted and unrestricted pathological trophoblast invasion.

Chorionic Villi↗