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

We studied the effect of atorvastatin on the adhesive phenotype of human endothelial cells (HUVEC) stimulated by tumor necrosis factor (TNF)-alpha. Surface expression of adhesion molecules on HUVEC was examined by flow cytometry and confocal microscopy, and adhesion of monocytes (human THP-1 cell line) was measured in vitro under flow conditions. In TNF-alpha-activated HUVEC, atorvastatin significantly enhanced surface expression of vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, E-selectin, and fractalkine, when compared with TNF-alpha stimulation alone. This enhancement was reversed by mevalonate or geranylgeranyl pyrophosphate (GGPP) and was mimicked by an inhibitor of geranylgeranylation. The enhancing effect of atorvastatin was restricted to TNF-alpha-inducible adhesion molecule and was the reflect of an increased protein synthesis (mRNA and protein) and not of a reduced shedding. Confocal microscopy examination showed that atorvastatin also altered the surface distribution of adhesion molecules. Adhesion of human THP-1 cells on TNF-alpha-activated HUVEC was significantly reduced by atorvastatin (-42% at 1 microM). Mevalonate or GGPP restored the TNF-alpha-induced adhesive potential. These results show that atorvastatin, by inhibiting prenylation of G proteins, enhances the TNF-alpha-induced expression of adhesion molecules at the endothelial cell surface and also alters their surface distribution which may account for the reduced binding of monocytes.
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PMID:Effect of atorvastatin on adhesive phenotype of human endothelial cells activated by tumor necrosis factor alpha. 1254 94

Leukocyte beta2 integrins Mac-1 and p150,95 are promiscuous cell-surface receptors that recognise and mediate cell adhesion to a variety of adsorbed and denatured proteins. We used albumin as a model protein to study whether leukocyte adhesion and activation depended on the nm-scale topography of a protein adlayer. Albumin adsorbed from the native conformation gave rise to different adlayer topographies and different amounts of adsorbed protein on hydrophobic and relatively hydrophilic polystyrene and silanised silicon-wafer surfaces, whereas adsorption of pre-denatured Alb resulted in similar adlayer topographies and similar amounts of adsorbed protein on these surfaces. All three distinct protein-adlayer topographies supported adhesion of in vitro differentiated, macrophage-like U937 and THP-1 cells, but did not support adhesion of their promonocytic precursors. Human monocytes freshly isolated from peripheral blood did not adhere to adsorbed albumin, not even in the presence of monocyte chemoattractant protein-1 and macrophage inflammatory protein-1alpha chemokines. Adhesion of the macrophage-like cells to albumin in any of the three topographies was inhibited by antibodies against beta2 integrins, but not by antibodies against beta1 integrins, and did not induce secretion of the proinflammatory cytokine tumour necrosis factor-alpha.
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PMID:The recognition of adsorbed and denatured proteins of different topographies by beta2 integrins and effects on leukocyte adhesion and activation. 1560 99

Adhesion is a fundamental cellular response that is essential to the physiologic processes of development, differentiation, proliferation, and motility, as well as to the pathology of inflammation, transformation, and metastasis. Adhesion of phagocytic leukocytes is a critical modulator of antimicrobial and cytotoxic functions, including the respiratory burst, secretion, and apoptosis. Because phospholipase D (PLD) is linked to several signaling pathways implicated in these processes, we tested the hypothesis that PLD regulates phagocyte adhesion. Adhesion of primary human neutrophils and monocyte-derived macrophages to fibronectin was accompanied by marked stimulation of PLD activity. Similarly, adhesion of both human (PLB, THP-1) and murine (RAW) myeloid-macrophage cell lines to fibronectin, fibrinogen, collagen, or plastic resulted in significant activation of PLD. Stimulation of PLD activity was rapid and persisted for at least 90 min. Confocal microscopy indicated that PLD1 exhibited partial colocalization with actin filaments at the adherent interface, in proximity to the focal adhesion protein, paxillin. Reductions in PLD activity by chemical inhibitors or specific short-interfering RNA-induced knockdown of PLD1 resulted in significant inhibition of phagocyte adhesion and was accompanied by reductions in total cellular F-actin. These data support the hypotheses that adhesion stimulates PLD activity, and that PLD1 regulates the initial stages of phagocyte adhesion. Stimulation of PLD activity may promote adhesion-dependent phagocyte effector responses.
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PMID:Phospholipase D1 regulates phagocyte adhesion. 1651 37

Candida albicans is considered the main pathogenic yeast responsible for a multitude of infective disorders. However, other yeasts, such as Candida famata, are being recognized as potential emerging pathogens that cause several types of infections in humans and animals. Consequently, we have investigated the adhesion and internalization of Candida famata into monocytes and epithelial cells. The interaction of the yeast with the cells is very rapid and takes place during the first 15 min of injection. However, the affinity of the yeast for the cells varies, THP-1 (human monocytes) being the highest and followed in decreasing order by HeLa (human carcinoma), HaCaT, and Pam-212 (human and mouse keratinocytes, respectively). Heat inactivation or treatment with nystatin, significantly decreases yeast adhesion to cells. Immunofluorescence, as well as scanning and transmission electron microscopy, reveals that cell lines are able to internalize C. famata. At 48 h after infection, most of the yeasts located inside cells appear degraded, but some yeasts recovered from lysed cells, were still viable. Adhesion and internalization of C. famata into HeLa cells were found to be lower than those of C. albicans and C. glabrata, but higher than those of S. cerevisiae. In addition, infection with C. famata results in actin microfilaments rearrangement. This article presents novel data in the interaction of this pathogenic yeast with mammalian cells.
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PMID:Attachment and entry of Candida famata in monocytes and epithelial cells. 1766 91

Intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) play critical roles in mediating monocyte adhesion to the vascular endothelium and monocyte migration into the subendothelial regions of the vessels. Inasmuch as cardiotrophin-1 (CT-1), an IL-6-type cytokine, was expressed in human atherosclerotic plaque, we examined whether CT-1 induces monocyte adhesion and migration by stimulating gene and protein expressions of ICAM-1 and MCP-1 in human aortic endothelial cells (HAECs). Immunocytochemistry revealed that CT-1 increased intensity of ICAM-1 and MCP-1 immunoreactivity in HAECs. Adhesion assay and chemotaxis assay revealed that CT-1 increased human monocytic THP-1 cell adhesion to HAECs and promoted chemotaxis in THP-1 cells, which were attenuated by anti-ICAM-1 and anti-MCP-1 antibody, respectively. Western blot analysis showed that CT-1 increased phosphorylation of ERK1/2 MAP kinase, p38 MAP kinase, and Akt and that their inhibitors, PD-98059, SB-203580, and LY-294002, respectively, inhibited phosphorylation. RNase protection assay and ELISA demonstrated that CT-1 increased gene and protein expressions of ICAM-1 and MCP-1. EMSA revealed that CT-1 enhanced NF-kappaB DNA-binding activity. CT-1-mediated upregulation of ICAM-1 and MCP-1 was suppressed by PD-98059, SB-203580, LY-294002, and parthenolide. The present study demonstrates that CT-1 promotes monocyte adhesion and migration by stimulating ICAM-1 and MCP-1 through mechanisms that involve ERK1/2 MAP kinase, p38 MAP kinase, phosphatidylinositol 3-kinase, and NF-kappaB pathways and suggests that CT-1 plays an important role in the pathophysiology of vascular inflammation and atherosclerosis.
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PMID:Cardiotrophin-1 stimulates intercellular adhesion molecule-1 and monocyte chemoattractant protein-1 in human aortic endothelial cells. 1805 23

Adhesion molecules have been implicated in the development and progression of cardiovascular disease, which is highly prevalent in people with diabetes. Adhesion molecules can mediate adhesion of leukocytes to the endothelium. Furthermore, P-selectin expressed on platelets is able to mediate the adhesion of leukocytes to platelets. In this study, we examine the in-vivo and in-vitro effects of rosiglitazone with particular emphasis on three important adhesion molecules (VCAM-1, ICAM-1 and P-selectin). In the aorta of STZ-diabetic apolipoprotein E-deficient (apoE KO) mice, rosiglitazone significantly reduced both total and arch plaque area. The mechanism for this appeared to be reduced macrophage infiltration into the atherosclerotic plaque which was also associated with reduced mRNA levels for VCAM-1, ICAM-1, MCP-1 and P-selectin in the aorta. In-vitro studies revealed reduced cell adhesion of monocytic cells (THP-1) to fibrinogen and endothelial cells (HUVEC) after incubation with rosiglitazone. Furthermore, the reduction in leukocyte adhesion also correlated with significant reductions in mRNA levels for VCAM-1, ICAM-1 and P-selectin indicating that reduced macrophage infiltration in atherosclerotic plaques may occur as a result of a direct effect of rosiglitazone on adhesion molecules in both monocytes and endothelial cells. Thus, we have shown that rosiglitazone appears to have direct anti-atherosclerotic effects in an animal model of diabetes-associated atherosclerosis which are at least partly due to effects on VCAM-1, ICAM-1, MCP-1 and P-selectin expression which leads to decreased leukocyte adhesion and macrophage infiltration.
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PMID:Reduced plaque formation induced by rosiglitazone in an STZ-diabetes mouse model of atherosclerosis is associated with downregulation of adhesion molecules. 1809 96

Mimicking the in vivo stem cell niche to increase stem cell expansion will likely require the presentation of multiple ligands. Presenting ligands in fluid-supported lipid monolayers (SLMs) or bilayers (SLBs) allows for ligand diffusion to complement the arrangement of cell receptors as well as cell-mediated ligand rearrangement and clustering. Cells in tissues interact with ligands presented by other cells and the extracellular matrix (ECM), so it will likely be beneficial to present both cell-associated and ECM-derived ligands. A number of investigators have incorporated cell-membrane-associated ligands within fluid surfaces, and several groups have shown that these ligands cluster beneath the cells. However, few studies have investigated cell adhesion to ECM-derived ligands in fluid surfaces. Fibronectin is an important ECM component in many tissues, including the hematopoietic stem cell niche. We examined the adhesion of the M07e and THP-1 hematopoietic progenitor cell lines to fibronectin-derived peptide ligands for the alpha5beta1 (cyclic and linear RGD) and alpha4beta1 (cyclic LDV) integrins as well as the heparin-binding domain (HBD) presented as lipopeptides in fluid and gel SLMs. M07e cells adhered more avidly than THP-1 cells to all of the lipopeptides in fluid and gel surfaces. The adhesion of both cell lines to all peptides was less avid in fluid versus gel SLMs. Adhesion to cyclic LDV (cLDV) and cRGD was similar on gel SLMs for both cell lines. In contrast, adhesion to cLDV was less extensive than to cRGD in fluid SLMs, especially for M07e cells. Adhesion to linear RGD was less avid than to cRGD or cLDV and decreased to a greater extent in fluid SLMs. Human aortic endothelial cells adhered to cRGD in fluid SLMs and remained viable for at least 24 h but did not spread. We also showed additive THP-1 cell adhesion to cLDV and linear RGD lipopeptides presented in a fluid SLM. Although DOPC (dioleoyl phosphatidyl choline) SLMs are not sufficiently stable for long-term cell culture studies, our results and those of others suggest that fluid SLMs are likely to be useful for presenting multiple ligands and for mimicking short-term interactions in the stem cell niche.
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PMID:Effects of supported lipid monolayer fluidity on the adhesion of hematopoietic progenitor cell lines to fibronectin-derived peptide ligands for alpha5beta1 and alpha4beta1 integrins. 1943 69

Adhesion molecules play an important role in the pathogenesis of atherogenesis. They are expressed on endothelial cells surface in response to various inflammatory stimuli. In this paper, we examined the effect of 2-tellurium-bridged beta-cyclodextrin (2-TeCD), a GPx mimic, on the expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs) under tumor necrosis factor-alpha (TNF-alpha) stimulation. Experimental results indicated that 2-TeCD suppressed the TNF-alpha-induced the expression of vascular adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1) on HUVECs surface in a dose-dependent manner. 2-TeCD also reduced the level of mRNA expression of VCAM-1 and ICAM-1. Furthermore, 2-TeCD inhibited THP-1 monocyte adhesion to HUVECs stimulated by TNF-alpha. Nuclear factor-kappaB (NF-kappaB) could regulate transcription of VCAM-1 and ICAM-1 genes. Western blot analysis showed that 2-TeCD inhibited the translocation of the p65 subunit of NF-kappaB into the nucleus. In short, these results indicated that 2-TeCD inhibits TNF-alpha-stimulated VCAM-1 and ICAM-1 expression in HUVECs partly due to suppressing translocation of NF-kappaB.
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PMID:Effect of 2-TeCD on the expression of adhesion molecules in human umbilical vein endothelial cells under the stimulation of tumor necrosis factor-alpha. 1943 96

In this study, we analyzed the probiotic potential of L. plantarum DSMZ 12028 in vitro using the pathogen E. coli K4 and a certified probiotic, L. paracasei F19, as controls. Adhesion to intestinal epithelial cells was evaluated using two cell lines, CaCo-2 and HT-29, through the plate dilution method. Moreover, the bacteria/epithelial dynamic interaction was continuously monitored using time-lapse microscopy. Expression of the innate immunity receptors, the TLRs, was evaluated by semi-quantitative PCR on an epithelial/bacteria co-culture. Real-time PCR was used to monitor expression of TLRs and cytokines in a monocytic cell line (THP-1) following bacterial exposure. The adherence of the strain to intestinal epithelial cells was comparable to that of the probiotic. Time-lapse experiments showed that E. coli K4 induced cell death while L. plantarum did not affect proliferation at a 10:1 bacteria/cell ratio. L. plantarum down-regulated TLR mRNAs with the exception of TLR2, while L. paracasei F19 and E. coli K4 caused a significant (p<0.05) up-regulation of TLR2 and 4, respectively. To simulate the activation of underlying immune cells in the lamina propria, we analyzed the immunomodulation of L. plantarum on a monocytic cell line, THP-1. Proinflammatory cytokines, such as TNFalpha, were increased by the presence of bacteria. The pathogen E. coli K4 also induced a strong up-regulation of proinflammatory cytokines, such as IL8, IL1beta and IL23. No differences were observed between experimental groups for IFNgamma, IL-10 and IL12p40. Overall, L. plantarum DSMZ 12028 demonstrated probiotic traits, inducing a proinflammatory response just above the "threshold level", which could prevent an inflammatory outcome, while inducing a higher state of alertness in the defense system of the host intestinal epithelial cells.
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PMID:In vitro evaluation of Lactobacillus plantarum DSMZ 12028 as a probiotic: emphasis on innate immunity. 1974 96

The mechanism that is responsible for progression of atherosclerosis seen with increasing age remains controversial. This issue was addressed in the present study, by searching for genes that are uniquely expressed in senescent endothelial cells and functionally involved in inflammatory leukocyte adhesion recognized as a critical step in the initiation of atherogenesis. Senescent human umbilical vein endothelial cells (HUVECs) prepared by continuous subculturing in vitro showed higher binding affinity for monocytes (THP-1 cells, human acute monocytic leukemia cell line) compared with young cells. Gene expression profiles between young and senescent endothelial cells were compared by the cDNA microarray method, and CD44 was identified as one of the "senescence-induced cell adhesion genes" whose expression was upregulated in senescent cells and whose gene ontology annotation indicated their role in cell adhesion. The enhanced gene expression of CD44 in senescent endothelial cells was verified both at the mRNA and protein levels. Adhesion of monocytes to senescent endothelial cells was significantly reduced following pretreatment of endothelial cells with the CD44 antibody or small-interfering RNA, thus reinforcing the critical role of CD44 in the inflammatory event. Exogenous expression of CD44 in young HUVECs and in human aortic endothelial cells led to an increase in monocyte adhesion. CD44 expression levels in the rat aorta endothelium were found to increase in an age-dependent manner, as determined by immunohistochemistry and Western blotting. CD44 and other senescence-induced cell adhesion genes identified in this study may provide the novel targets for the prevention of inflammatory leukocyte adhesion leading to the development atherosclerosis.
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PMID:Identification of CD44 as a senescence-induced cell adhesion gene responsible for the enhanced monocyte recruitment to senescent endothelial cells. 2038 54


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