Disease relevance of Chorionic Villi

• BACKGROUND: Screening for trisomy 21 (Down's syndrome) by measuring maternal serum alpha-fetoprotein, chorionic gonadotropin, and estriol concentrations and then performing chorionic-villus sampling or amniocentesis identifies approximately 60 percent of fetuses with this disorder [1].
• A pregnancy at risk for adenosine deaminase deficiency and severe combined immunodeficiency disease was investigated using samples of chorionic villi obtained during the eighth week of pregnancy [2].
• Heteroduplex mobility assay analysis showed the presence of multiple HIV-1 env quasispecies in sequential maternal peripheral blood mononuclear cell samples, but only a small number of env variants were found in chorionic villi and enriched trophoblastic cells [3].
• Prenatal diagnosis of nonketotic hyperglycinemia: enzymatic analysis of the glycine cleavage system in chorionic villi [4].
• Using cultured trophoblast cells obtained by chorionic villus biopsy, we diagnosed Fanconi anemia (FA) in two pregnancies and excluded it in eight pregnancies at risk for the syndrome [5].

High impact information on Chorionic Villi

• Levels of annexin V, a phospholipid-binding protein with potent anticoagulant activity, are markedly reduced on placental villi from women with this syndrome [6].
• DNA analysis can be performed in amniocytes or chorionic-villus cells to identify mutations of the dystrophic gene prenatally, but immunochemical testing for dystrophin cannot be performed because the protein is not expressed in these cells [7].
• Prenatal diagnosis of cytochrome c oxidase deficiency by biopsy of chorionic villi [8].
• Predictions can be made directly from chorionic villi, without previous DNA extraction, and fetal sex can be determined by amplification of sequences specific for the Y chromosome [9].
• Distribution of beta2 microglobulin and HLA in chorionic villi of human placentae [10].

Chemical compound and disease context of Chorionic Villi

• The prevalence of chorionic villus hemorrhage among women using cocaine also was 17% [11].
• Fetal demise with Smith-Lemli-Opitz syndrome confirmed by tissue sterol analysis and the absence of measurable 7-dehydrocholesterol Delta(7)-reductase activity in chorionic villi [12].
• Prenatal diagnosis of cystinosis by quantitative measurement of cystine in chorionic villi and cultured cells [13].
• We conclude that digit anomalies in the offspring of A/J mice result from fetal vascular disruptive phenomena subsequent to maternal blood loss induced hypovolemia and hypoperfusion to the uterus and placenta as has been suggested for uterine vascular clamping, misoprostol, chorionic villus sampling, and cocaine teratogenesis [14].
• Prenatal diagnosis of Pompe's disease (type II glycogenosis) in chorionic villus biopsy using maltose as a substrate [15].

Biological context of Chorionic Villi

• First trimester chromosomal analysis of complex structural rearrangements with RHA banding on chorionic villi [16].
• We have previously shown that the glucose-6-phosphate dehydrogenase (G6PD) locus (G6PD) on the allocyclic X chromosome in chorionic villi is partially expressed [17].
• PDGF-A expression was also detected in columnar cytotrophoblasts where it may have a potential role in stimulating mesenchymal cell growth at the base of the growing placental villi [18].
• Restriction fragment length polymorphism analysis of the PstI KM19 site revealed that the cftr locus was identical in the chorionic villi and in CFI-3 cells [19].
• To investigate the role of retinoids on human placental development and functions, we characterized the spatial distribution of retinoid receptors in human term chorionic villi [20].

Anatomical context of Chorionic Villi

• In situ hybridization and immunocytochemistry revealed that AT1 receptor mRNA and protein were localized throughout pregnancy in the cytotrophoblast, syncytiotrophoblast, and extravillous trophoblast, as well as in or around the blood vessels of placental villi [21].
• Our data suggest that DS is in a position to activate HCII in the fetal blood vessels or in the stroma of placental villi after injury to the syncytiotrophoblast layer and thereby inhibit fibrin generation in the placenta [22].
• Fibroblasts, chorionic villi and hair roots showed the highest level of FMR2 expression, whole blood cells and amniocytes showed very low expression, and the transcript was not detected in lymphoblasts [23].
• Syncytiotrophoblasts were defined using anti-cytokeratin mAb (AE1/3), whereas endothelial cells in placental villi were distinctly identified using a mAb directed to CD31 [24].
• Our inference, that Fc gamma RIIb was the likely receptor, we confirmed by analyzing purified placental villi, enriched in endothelium, by immunoblotting with a new Ab specific for the cytoplasmic tail of Fc gamma RIIb [25].

Associations of Chorionic Villi with chemical compounds

• Extraction of fibronectin from two human tissues, lung parenchyma and placental villi, was facilitated by the incorporation of heparin into extraction media [26].
• Vascular disruptive syndromes after exposure to misoprostol or chorionic villus sampling [27].
• Electron microscope autoradiography has been used to study protein synthesis in syncytial and cellular trophoblast of term human placental villi incubated in vitro with tritiated leucine ([3H]leu) [28].
• Kinetic analysis, isolation, and characterization of hydrophilic folate-binding proteins released from chorionic villi cultured under serum-free conditions [29].
• Thromboxane and prostacyclin production by different compartments of the human placental villus [30].

Gene context of Chorionic Villi

• As part of an effort to define the local effects of the placentally expressed members of the GH/Prl family of hormones on the placenta, we have identified an isoform (hGHRd3) of the growth hormone receptor expressed in the placental villi. hGHRd3 mRNA differs from the liver GHR mRNA by the deletion of a 66-base pair segment encoding exon 3 [31].
• It was also expressed in the trophoblasts of the cytotrophoblastic shell and Langhan's layer of placental villi only in the first trimester, suggesting an autocrine role for IGF-II in early cytotrophoblastic proliferation and/or differentiation [32].
• SDFs were transfected in vitro into cells obtained from five human fetal chorionic villi of embryos, homozygous for the SMN1 deletion, by either electroporation or microinjection [33].
• Early placentae were also found to contain both DAF+ and DAF- chorionic villi [34].
• Relationship between tissue damage and heme oxygenase expression in chorionic villi of term human placenta [35].

Analytical, diagnostic and therapeutic context of Chorionic Villi

• Northern blotting revealed that ADM mRNA (1.3 kb) was expressed in chorionic villi and basal plate regions, but was most abundantly expressed in the choriodecidua [36].
• Interleukin-1 beta treatment of placental villi or coculture of villous core mesenchymal cells with isolated trophoblast cells did not stimulate HGF production [37].
• Direct sequence analysis of genomic DNA from the affected father and from both chorionic villus samples revealed a tyrosine to asparagine mutation at position 14 within the highly conserved 1A alpha-helical segment of keratin 10 [38].
• The chorionic villi were obtained 4 h after exposure and activation of caspase-3 and cytochrome c release were analyzed by Western blotting [39].
• RESULTS: Immunofluorescence staining with proMBP absorbed anti-PAPP-A antibody showed that PAPP-A is localized to placental septa, anchoring villi, and the syncytia of chorionic villi, whereas MBP is localized only to septa and anchoring villi [40].

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