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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies of spinal cord development and plasticity, in chick, have demonstrated a loss of regenerative ability correlating to embryonic day (E) 13 of the 21-day developmental period. Here we describe membrane fractions from embryonic chick spinal cords as permissive or restrictive substrates for the neuron-like differentiation of neuroblastoma x glioma hybrid NG108-15 cells, in vitro. Plasma membranes were purified from the thoracic spinal cord of embryos at a series of developmental stages (E10-E18). Micro-well plates were coated with the fractions and NG108-15 cells cultured thereon. Cells adhered to the E10-coated wells and began to differentiate after 2 h, becoming highly differentiated, with neurites 2-3 times longer than the diameter of the cell body after 24 h in in culture. In contrast, cells cultured in E18-coated wells remained as clusters of undifferentiated cells of rounded morphology, even after 48 h in culture. As well, the permissive and restrictive plasma membranes were assessed semiquantitatively as the number of adhering cells after 20 h of culture. Adhesion of cells to the substrate decreased as the embryonic age of the plasma membrane substrate increased. Examination of the plasma membrane fractions, using SDS-PAGE, revealed several proteins in the 40-60 kDa range that varied substantially between E12, E14 and E18. Results of this study provide in vitro confirmation of previous in vivo findings; namely, that early embryonic spinal cord is initially permissive for neuritic outgrowth becoming restrictive around E13.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Developmental transition by spinal cord plasma membranes of embryonic chick from permissive to restrictive substrates for the morphological differentiation of neuroblastoma x glioma hybrid NG108-15 cell. 845 60

E-cadherin is a cell-cell adhesion molecule and tumor invasion suppressor gene that is frequently altered in human cancers. It interacts through its cytoplasmic domain with beta-catenin which in turn interacts with the Wnt (wingless) signaling pathway. We have compared the effects of different tumor-derived E-cadherin variants with those of normal E-cadherin on Wnt signaling and on genes involved in epithelial mesenchymal transition. We established an in-house cDNA microarray composed of 1105 different, sequence verified cDNA probes corresponding to 899 unique genes that represent the majority of genes known to be involved in cadherin-dependent cell adhesion and signaling ('Adhesion/Signaling Array'). The expression signatures of E-cadherin-negative MDA-MB-435S cancer cells transfected with E-cadherin variants (in frame deletions of exon 8 or 9, D8 or D9, respectively, or a point mutation in exon 8 (D370A)) were compared to that of wild-type E-cadherin (WT) transfected cells. From the differentially expressed genes, we selected 38 that we subsequently analyzed by quantitative real-time RT-PCR and/or Northern Blot. A total of 92% of these were confirmed as differentially expressed. Most of these genes encode proteins of the cytoskeleton, cadherins/integrins, oncogenes and matrix metalloproteases. No significant expression differences of genes downstream of the Wnt-pathway were found, except in E-cadherin D8 transfected cells where upregulation of three Tcf/Lef-transcribed genes was seen. One possible reason for the lack of expression differences of the Tcf/Lef-regulated genes is upregulation of SFRP1 and SFRP3; both of which are competitive inhibitors of the Wnt proteins. Interestingly, known E-cadherin transcriptional repressors, such as SLUG (SNAI2), SIP1 (ZEB2), TWIST1, SNAIL (SNAI1) and ZEB1 (TCF8), but not E12/E47 (TCF3), had a lack of upregulation in cells expressing mutated E-cadherin compared to WT. In conclusion, E-cadherin mutations have no influence on expression of genes involved in Wnt-signaling, but they may promote their own expression by blocking upregulation of E-cadherin repressors.
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PMID:Tumor-associated E-cadherin mutations do not induce Wnt target gene expression, but affect E-cadherin repressors. 1531 Dec 12

Increased nuchal translucency in the human fetus is associated with chromosomal abnormalities, enlarged jugular lymphatic sacs, cardiac defects and changed flow through the ductus venosus. The developmental background of this nuchal edema in relation to the associated anomalies remains elusive. We studied the morphologic correlation between neurogenesis and vasculogenesis in neck, heart, and ductus venosus region of wild type and trisomy 16 mice embryos (E10- E18), using an antibody against Neural Cell Adhesion Molecule (NCAM). Trisomy 16 mice are a model for the above described human phenotype. From E12 trisomy 16 mice showed an altered arrangement of cranial nerves IX, X and XI, which are positioned between the carotid artery, jugular vein and enlarged lymphatic sac. The vagal nerve was significantly smaller, compared with wild type embryos. NCAM was over expressed in both neuronal and cardiovascular structures in trisomy 16 mice, being particularly prominent in the 4th and 6th pharyngeal arch arteries, and the ductus venosus. In the 4th and 6th pharyngeal arch arteries, NCAM over expression was located to the part of the vessel wall that is closely related to the vagal and recurrent nerve. In case of 4th pharyngeal arch artery abnormalities NCAM expression, on the other hand, was reduced. In conclusion, the interaction between neurogenesis and vasculogenesis is disturbed in the trisomy 16 mouse model, and might be a common denominator in the spectrum of anomalies associated with increased nuchal translucency.
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PMID:Increased NCAM expression and vascular development in trisomy 16 mouse embryos: relationship with nuchal translucency. 1630 97

The HT29MTXE12 (E12) cell line harbors an adherent mucus layer, providing a novel technique to model mucosal infection in vitro. In this study, we have characterized the interaction of Campylobacter jejuni with the E12 cell line and exploited its unique mucus layer to examine the potential efficacy of probiotic treatment to attenuate C. jejuni virulence properties. C. jejuni 81-176 colonized and reproduced in E12 mucus. Adhesion to and internalization of C. jejuni were enhanced in E12 cells harboring mucus compared to parental cells without mucus. Translocation of C. jejuni occurred at early time points following infection. C. jejuni aligned with tight junctions and colocalized with the tight junction protein occludin, suggesting a paracellular route of translocation. Probiotic strains Lactobacillus rhamnosus R0011, Lactobacillus helveticus R0052, Lactobacillus salivarius AH102, Bifidobacterium longum AH1205, a commercial combination of L. rhamnosus R0011 and L. helveticus R0052 (Lacidofil), and a cocktail consisting of L. rhamnosus, L. helveticus, and L. salivarius (RhHeSa) colonized E12 mucus and bound to underlying cells. Probiotics attenuated C. jejuni association with and internalization into E12 cells and translocation to the basolateral medium of transwells. Live bacteria and prolonged precolonization of E12 cells with probiotics were necessary for probiotic action. These results demonstrate the potential for E12 cells as a model of mucosal pathogenesis and provide a rationale for the further investigation of probiotics as prophylaxis against human campylobacteriosis.
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PMID:Probiotic colonization of the adherent mucus layer of HT29MTXE12 cells attenuates Campylobacter jejuni virulence properties. 2030