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

Adhesion molecules of the integrin beta1 family are thought to be involved in the malignant progression renal cell carcinoma (RCC). Still, it is not clear how they contribute to this process. Since the hematogenous phase of tumour dissemination is the rate-limiting step in the metastatic process, we explored beta1 integrin alterations on several RCC cell lines (A498, Caki1, KTC26) before and after contacting vascular endothelium in a tumour-endothelium (HUVEC) co-culture assay. Notably, alpha2, alpha3 and alpha5 integrins became down-regulated immediately after the tumour cells attached to HUVEC, followed by re-expression shortly thereafter. Integrin down-regulation on RCC cells was caused by direct contact with endothelial cells, since the isolated endothelial membrane fragments but not the cell culture supernatant contributed to the observed effects. Integrin loss was accompanied by a reduced focal adhesion kinase (FAK) expression, FAK activity and diminished binding of tumour cells to matrix proteins. Furthermore, intracellular signalling proteins RCC cells were altered in the presence of HUVEC membrane fragments, in particular 14-3-3 epsilon, ERK2, PKCdelta, PKCepsilon and RACK1, which are involved in regulating tumour cell motility. We, therefore, speculate that contact of RCC cells with the vascular endothelium converts integrin-dependent adhesion to integrin-independent cell movement. The process of dynamic integrin regulation may be an important part in tumour cell migration strategy, switching the cells from being adhesive to becoming motile and invasive.
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PMID:Transient down-regulation of beta1 integrin subtypes on kidney carcinoma cells is induced by mechanical contact with endothelial cell membranes. 1776 Aug 43

The initial steps of Salmonella pathogenesis involve adhesion and invasion of host epithelial cells. While well-studied for S Typhimurium, the factors contributing to this process in other, host-adapted serovars remains unexplored. Here, we screened clinical isolates of serovars Gallinarum, Dublin, Choleraesuis, Typhimurium and Enteritidis for adhesion and invasion of intestinal epithelial cell lines of human, porcine, and chicken origins. 30 isolates with altered infectivity were used for genomic analyses and 14 genes and novel mutations associated with high or low infectivity were identified. The functions of candidate genes included virulence gene expression regulation, cell wall or membrane synthesis and components. The role of several of these genes in Salmonella adhesion and invasion to cells has not previously been investigated. The genes dksA (stringent response regulator) and sanA (vancomycin high-temperature exclusion protein) were selected for further analyses, and we confirmed their roles in host cell adhesion and invasion. Furthermore, transcriptomic analyses were performed for S Enteritidis and S Typhimurium, with two highly infective and two marginally infective isolates for each serovar. Expression profiles for the isolates with altered infection phenotypes revealed the importance of T3SS expression levels in the determination of isolate's infection phenotype. Taken together, these data indicate a new role in cell host infection for genes or gene variants previously not associated with adhesion and invasion to the epithelial cells.Importance Salmonella is a foodborne pathogen affecting over 200 million people and resulting in over 200,000 fatal cases per year. Adhesion to and invasion of Salmonella into intestinal epithelial cells is one of the first and key steps in the pathogenesis of salmonelosis. Still, around 35-40% of bacterial genes have no experimentally validated function and their contribution to the bacterial virulence, including adhesion and invasion, remains largely unknown. Therefore the significance of this study is in the identification of new genes or gene allelic variants previously not associated with adhesion and invasion. It is well established that blocking adhesion and/or invasion would stop or hamper bacterial infection, therefore the new findings from this study could be used in future developments of anti-Salmonella therapy targeting genes involved in these key processes. Such treatment could be a valuable alternative as the numbers of antibiotic-resistant bacteria is growing very rapidly.
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PMID:Identification of natural mutations responsible for altered infection phenotypes of Salmonella enterica clinical isolates using cell line infection screens. 3312 19

Adhesion between two bodies is a key parameter in wear processes. At the macroscale, strong adhesive bonds are known to lead to high wear rates, as observed in clean metal-on-metal contact. Reducing the strength of the interfacial adhesion is then desirable, and techniques such as lubrication and surface passivation are employed to this end. Still, little is known about the influence of adhesion on the microscopic processes of wear. In particular, the effects of interfacial adhesion on the wear particle size and on the surface roughness evolution are not clear and are therefore addressed here by means of molecular dynamics simulations. We show that, at short timescales, the surface morphology and not the interfacial adhesion strength dictates the minimum size of wear particles. However, at longer timescales, adhesion alters the particle motion and thus the wear rate and the surface morphology.
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PMID:Role of interfacial adhesion on minimum wear particle size and roughness evolution. 3321 20