[Acid etch and adhesives in dentistry II. Adhesion--capillarity--superficial tension--surfaces of high and low energy--high adhesion].
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Acid Etching, Dental↗
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[Adhesion mechanisms of adhesives and composites (or how do adhesive and composites adhere?)].
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Acid Etching, Dental↗
[The clinical application of a new adhesive resin (MMA-4-META-TBB-O) to an adhesion bridge (adhesion splint) (author's transl)].
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Acrylic Resins↗
Monocyte adhesion and adhesion molecule expression on human endothelial cells on plasma-treated PET and PTFE in vitro.
The aim of this study was to evaluate in vitro the inflammatory potential of endothelialized surfaces of polyethylene terephthalate (PET) and polytetrafluorethylene (PTFE) after ammonia gas plasma modification. HUVECs grown on polystyrene and HUVECs stimulated with tumor necrosis factor (TNF-alpha) were used as controls. At day 1 and day 7, surfaces were evaluated for U937 cells and HUVECs using flow cytometry and immunohistochemistry. Plasma-treated PET (T-PET) and treated PTFE (T-PTFE) increased U937 cell adhesion compared to the negative control but this was not statistically significant. Maximal adhesion of U937 cells to HUVEC was observed on TNF-alpha stimulated endothelium with significant differences between day 1 and day 7. There was a small increase in U937 cell adhesion to plasma-treated PET compared to PTFE on both day 1 and day 7, but this was not statistically significant. Immunohistochemical staining demonstrated two patterns of distribution for monocyte adhesion on materials. On T-PET the cells were positioned in clusters attached to HUVECs and on T-PTFE the cells were randomly distributed on HUVECs and material. The effects of plasma-treated PET and PTFE on HUVEC adhesion and proliferation were also studied. On day 1 there were slight increases in the growth of HUVECs on both of T-PET and T-PTFE but this was not statistically significant. On day 7, cell number increased significantly on all of surfaces compared to the negative control. The results demonstrate that the plasma treatment of PET and PTFE with ammonia improves the adhesion and growth of endothelial cells and these surfaces do not exhibit a direct inflammatory effect in terms of monocyte adhesion. Plasma-treated PTFE enhances HUVECs growth and was less adhesive for monocytes as compared with treated PET. The monocyte adhesion to endothelial cells on surfaces can be used as a tool for the evaluation of material surface modification and further to study the mechanisms of cell to cell interactions in response to surfaces.
Journal Article↗
Fibronectin in an extracellular matrix of cultured endothelial cells supports platelet adhesion via its ninth type III repeat : A comparison with platelet adhesion to isolated fibronectin
We investigated the involvement of different domains of fibronectin in mediating platelet adhesion to fibronectin in the extracellular matrix (ECM) of cultured endothelial cells under flow conditions. Polyclonal anti-fibronectin antibodies were absorbed with Sepharose to which no protein, intact fibronectin, or different fibronectin fragments had been coupled to obtain supernatants (Sups) (Sup(0), Sup(FN), and Sup(name of the fragment), respectively) from which a specific part of the antibodies had been removed. Treatment of the ECM before perfusion with Sup(0) resulted in a 36% decrease in platelet coverage, whereas treatment with Sup(FN) resulted in maximal adhesion. Treatment of the ECM with supernatants from which antibodies directed against the gelatin- or heparin-binding domain had been removed showed the same inhibition as treatment with Sup(0). Removal of antibodies directed to the 120-kDa cell-binding domain resulted in a level of adhesion equal to the level found when the ECM was treated with Sup(FN). Further analysis of this central region showed that only treatment with supernatants from which antibodies directed to the ninth type III repeat (III-9) of fibronectin had been removed resulted in a significantly higher adhesion than treatment with Sup(0). Studies of adhesion to the fragments themselves showed that only fragments containing III-10 were able to support adhesion. Mutation of the Arg-Gly-Asp (RGD) sequence into Arg-Gly-Glu (RGE) in one of those fragments resulted in a complete loss of adhesive capacity. These data suggest that platelet adhesion to fibronectin in the ECM depends on III-9, whereas III-10 does not seem to be required. For platelet adhesion to isolated fibronectin, an intact RGD sequence seems to be crucial.
Journal Article↗
Influence of interchanging adhesive resins and self-etching primers on the mechanical properties of adhesive resins.
This study determined the influence of interchanging adhesive resins and self-etching primers on the mechanical properties of adhesive resins. Four commercially available two-step self-etching primer systems were used. To measure microtensile strength, 0.5-mm thick dumbbell-shaped slabs of each combination of adhesive resin and self-etching primer were prepared. After 24 hours storage in 37 degrees C distilled water, these specimens were subjected to microtensile testing at a crosshead speed of 1.0 mm/minute. Fourier transformation infrared spectroscopy was used to determine the degree of conversion. The percentage of residual double bonds, including pendant and monomeric double bonds, was calculated by comparing the obtained ratio against uncured adhesive resin. The degree of conversion of the adhesive resins was obtained by subtracting the %C=C from 100%. Two-way ANOVAs, followed by Tukey tests, were done. The microtensile strengths and degree of conversion varied with different combinations of self-etching primer and adhesive resin. Numerically, the highest microtensile strengths were obtained when the primer/adhesive resin combinations from the same manufacturer were used. When the different combinations of self-etching primers and adhesive resins were mixed, the microtensile strength and degree of conversion of the adhesive resins tended to decrease for some combinations. Within the limitations of this study, which was far removed from clinical situations, the role of the self-etching primers on the mechanical properties of adhesive resins should be considered to create an authentic resin-dentin interface.
Analysis of Variance↗
Activation of pyk2/related focal adhesion tyrosine kinase and focal adhesion kinase in cardiac remodeling.
Cellular remodeling during progression of dilation involves focal adhesion contact reorganization. However, the signaling mechanisms and structural consequences leading to impaired cardiomyocyte adhesion are poorly defined. These events were studied in tropomodulin-overexpressing transgenic mice that develop dilated cardiomyopathy associated with chronic elevation of intracellular calcium. Analysis of tropomodulin-overexpressing transgenic hearts by immunoblot and confocal microscopy revealed activation and redistribution of signaling molecules known to regulate adhesion. Calcium-dependent pyk2/related focal adhesion tyrosine kinase (RAFTK) showed changes in expression and phosphorylation state, similar to changes observed for a related downstream target molecule of pyk2/RAFTK termed focal adhesion kinase. Paxillin, the target substrate molecule for focal adhesion kinase phosphorylation, was redistributed in tropomodulin-overexpressing transgenic hearts with enhanced paxillin phosphorylation and cleavage. Certain aspects of the in vivo signaling phenotype including increased paxillin phosphorylation could be recapitulated in vitro using neonatal rat cardiomyocytes infected with recombinant adenovirus to overexpress tropomodulin. In addition, increasing intracellular calcium levels with ionomycin induced pyk2/RAFTK phosphorylation, and adenovirally mediated expression of wild-type pyk2/RAFTK resulted in increased phospho-pyk2/RAFTK levels and concomitant paxillin phosphorylation. Collectively, these results delineate a cardiomyocyte signaling pathway associated with dilation that has potential relevance for cardiac remodeling, focal adhesion reorganization, and loss of contractility.
Animals↗
Platelet-endothelial cell adhesion molecule-1 and CD146: soluble levels and in situ expression of cellular adhesion molecules implicated in the cohesion of endothelial cells in idiopathic inflammatory myopathies.
OBJECTIVE: Idiopathic inflammatory myopathies (IIM) are a heterogeneous group of diseases characterized by chronic inflammation of muscles. We investigated the role of cellular adhesion molecules implicated in the cohesion of endothelial cells in IIM. METHODS: In 22 patients with IIM we investigated plasma concentrations of soluble junctional adhesion molecules [platelet-endothelial cell adhesion molecule (sPECAM-1) and sCD146] and cellular adhesion molecules [sP-selectin, sE-selectin, intercellular adhesion molecule (sICAM-1), and vascular cell adhesion molecule (sVCAM-1)] implicated in leukocyte/endothelial cell interactions. Results were compared to a control group. Muscle biopsy samples from 8 out of 22 IIM patients were studied by immunohistochemistry for tissue expression of these molecules and compared to normal muscle samples. PECAM-1 and CD146 expression was also studied using immunoblots from muscle biopsies from 5 patients and 2 controls. RESULTS: We observed distinct patterns of soluble levels and in situ expression between dermatomyositis (DM), polymyositis (PM), and sporadic inclusion body myositis (s-IBM). PM samples showed significantly increased levels of sCD146, sPECAM-1, and s-ICAM1 and increased expression of CD146, CD31, and ICAM-1 in endothelial cells, whereas CD146 and ICAM-1 were also recorded in some muscle fibers. In DM, sE-selectin, sP-selectin, and sPECAM-1 were significantly increased, with abnormal expression of ICAM-1 in endothelial cells and perifascicular muscle fibers. In the small group of s-IBM samples, results were similar to PM, but the only significant increase was the level of sPECAM-1. Immunoblots confirmed increased expression of PECAM-1 and CD146 in all IIM muscles in comparison to controls, with the highest expression in PM and IBM samples. CONCLUSION: We observed abnormal increases of soluble levels of adhesion molecules implicated in endothelial cell junctions in PM (sCD146, sPECAM-1) and to a lesser extent in DM and s-IBM (sPECAM-1). We conclude that the distinctly different profiles between PM/s-IBM and DM reflect differences in the pathophysiological background of these diseases.
CD146 Antigen↗
IgG anti-endothelial cell autoantibodies from patients with systemic lupus erythematosus or systemic vasculitis stimulate the release of two endothelial cell-derived mediators, which enhance adhesion molecule expression and leukocyte adhesion in an autocrine manner.
OBJECTIVE: To investigate the ability of anti-endothelial cell antibodies (AECA) to modulate endothelial cell function. METHODS: The effects of purified IgG from 11 patients with systemic lupus erythematosus (SLE) and 4 patients with systemic vasculitis on the expression of adhesion molecules (intercellular adhesion molecule 1, vascular cell adhesion molecule 1, E-selectin) by human umbilical vein endothelial cells and on the adhesion of the human promyelocytic cell line U937 were examined in vitro. RESULTS: IgG from 6 of 8 AECA-positive SLE patients and 3 of 3 AECA-positive systemic vasculitis patients up-regulated adhesion molecule expression and leukocyte adhesion to endothelial cells. The 4 AECA-negative samples had no effect. Transfer experiments demonstrated that at later time points (2-8 hours) after AECA addition, endothelium-derived interleukin-1 (IL-1) accounted for the ability of AECA to increase leukocyte adhesion. However, even within very short times after addition of AECA (<30 minutes), endothelial cells released a distinct transferable mediator with similar effects. CONCLUSION: AECA in patients with SLE or systemic vasculitis may contribute to pathogenesis by increasing leukocyte adhesion to endothelial cells. AECA act by inducing the release of at least two endothelium-derived mediators, one (as-yet-unidentified) rapidly and another (IL-1) more slowly, both of which stimulate endothelial cells in an autocrine manner.
Antibodies, Blocking↗
High insulin exacerbates neutrophil-endothelial cell adhesion through endothelial surface expression of intercellular adhesion molecule-1 via activation of protein kinase C and mitogen-activated protein kinase.
AIMS/HYPOTHESIS: The association of insulin resistance and compensatory hyperinsulinaemia with increased coronary events in diabetic patients is poorly understood. There are few publications about the direct atherogenic actions of insulin on the endothelium compared with those on vascular smooth muscle cells. The aim of this study was to elucidate whether high insulin directly affects neutrophil-endothelial cell adhesion and surface expression of endothelial adhesion molecules. We also examined what intracellular mechanisms are involved in these events. METHODS: Studies of adhesion between neutrophils from healthy volunteers and human umbilical vein endothelial cells incubated in insulin-rich medium were carried out. Adhered neutrophils were quantified by measuring their myeloperoxidase activities and surface expression of endothelial adhesion molecules was examined using an enzyme immunoassay. RESULTS: High insulin enhanced neutrophil-endothelial cell adhesion with an increase in the expression of intercellular adhesion molecule-1 but not E-selectin or P-selectin. Both phenomena were attenuated by pretreatment with protein kinase C inhibitors and a mitogen activated protein kinase inhibitor. CONCLUSIONS/INTERPRETATION: These results suggest that hyperinsulinaemia causes vascular injury by directly exacerbating neutrophil-endothelial cell adhesion through increasing endothelial expression of intercellular adhesion molecule-1 via activation of protein kinase and mitogen activated protein kinase pathways.
Cell Adhesion↗
Interaction between mesothelial cells and macrophages in the initial process of pleural adhesion: ultrastructural studies using adhesion molecules.
Detachment of mesothelial cells is an early step in adhesion of the human pleura. To elucidate this process, we used adhesion molecules as the targets of primary antibody and performed immunohistochemical staining of the mesothelial cells that cover the surface of the sites of pleural adhesion and the macrophages that migrate from connective tissue. The surface of the adhesion site that was formed as a result of edematous and villiform elongation of the connective tissue underlying the visceral pleura was covered with mesothelial cells. However, there was partial detachment of the mesothelial cells caused by adherence to macrophages that had migrated from within the connective tissue, and that adherence was mediated by adhesion molecules. We demonstrated that both mesothelial cells and macrophages each express both CD54 and CD11a, important adhesion molecules. It was surmised that the detachment of the mesothelial cells is the result of interaction with the macrophages via those adhesion molecules and that over time it progresses to pleural adhesion.
Aged↗
Glucocorticoid-induced surface expression of annexin 1 blocks beta2-integrin adhesion of human eosinophils to intercellular adhesion molecule 1 surrogate protein.
BACKGROUND: Glucocorticoids attenuate the population of eosinophils and T lymphocytes in asthmatic airways. The decrease in airway eosinophilia is caused both by accelerated cell death and by induction of blockade of integrin adhesion. In this study, we examined the hypothesis that annexin 1 surface expression, which is upregulated by the glucocorticoid receptor, prevents integrin adhesion essential to cell migration by blocking intracellular translocation of cytosolic group IV phospholipase A2 (cPLA2). OBJECTIVE: To examine the relationship of the glucocorticoid on annexin 1 expression and the effect of blockade of annexin 1 activity on adhesion of human eosinophils in vitro. To determine the relationship between annexin 1surface expression and nuclear membrane translocation of cPLA2. METHODS: Eosinophils isolated from human peripheral blood were pretreated with fluticasone propionate (FP), and beta2-integrin adhesion was measured after stimulation with IL-5 or eotaxin. Effects of FP on cPLA2 expression, phosphorylation, and translocation were determined. The role of annexin 1 was examined by using annexin 1 blocking antibody and/or mimetic peptides. RESULTS: Fluticasone propionate decreased stimulated eosinophil adhesion and caused 4-fold increase in annexin 1 expression on the plasma membrane. Inhibition of adhesion by FP was blocked with annexin 1 blocking antibody. Annexin 1 N-terminal mimetic peptide also blocked beta2-integrin adhesion. Translocation of cPLA2 to the nuclear membrane was significantly blocked by incubation with FP. Blockade was reversed with annexin 1 blocking antibody. CONCLUSION: Blockade of beta2-integrin adhesion by glucocorticoid is regulated by annexin 1, which blocks cPLA2 translocation to nuclear membrane.
Androstadienes↗
Cilostazol inhibits high glucose-mediated endothelial-neutrophil adhesion by decreasing adhesion molecule expression via NO production.
OBJECTIVE: Endothelial-neutrophil adhesion is crucial for vascular injury, the major cause of diabetic vascular complications. On the other hand, platelet aggregation inhibitors, frequently used for diabetic patients with intermittent claudication, have been shown to decrease the incidence of atherosclerosis-mediated diseases (acute myocardial infarction and stroke). However, whether these agents act directly on the endothelial reactions to hyperglycemia remains unclear. Therefore, we examined their direct effects on endothelial-neutrophil adhesion and expression of endothelial adhesion molecules induced by high glucose. METHODS AND RESULTS: After human endothelial cells were cultured in high glucose medium, neutrophils from healthy volunteers were added and allowed to adhere for 30 min. Adhered neutrophils were quantified by measuring their myeloperoxidase (MPO) activities, and surface expression of endothelial adhesion molecules was determined with an enzyme immunoassay. Of the platelet aggregation inhibitors tested, only cilostazol significantly attenuated the adhesion through decreasing expression of intercellular adhesion molecule-1 (ICAM-1) and P-selectin. In addition, nitric oxide (NO) synthase inhibitors reduced the inhibitory effects of cilostazol, but a protein kinase C (PKC) activator did not. CONCLUSIONS: Cilostazol may act directly on endothelial cells to inhibit expression of adhesion molecules and neutrophil adhesion induced by high glucose through increasing NO production.
Cell Adhesion↗
Participation of high glucose concentrations in neutrophil adhesion and surface expression of adhesion molecules on cultured human endothelial cells: effect of antidiabetic medicines.
BACKGROUND: Atherosclerosis and vascular inflammation induced by hyperglycemia are important factors in the promotion of diabetic complications. One of the earliest events in the inflammatory process is increased binding of neutrophils to endothelial cells. Since vascular inflammation has been recently reported to be crucial for the onset of atherosclerosis-mediated serious diseases (acute myocardial infarction, stroke), in this study, we examined the effects of high glucose concentrations on endothelial-neutrophil cell adhesion and surface expression of endothelial adhesion molecules. We also evaluated the effects of various antidiabetic medicines on these events. METHODS: Human umbilical vein endothelial cells (HUVECs) were first cultured for 48 h in the glucose-rich medium, and neutrophils from healthy volunteers were then added and allowed to adhere for 30 min. Adhered neutrophils were quantified by measuring myeloperoxidase (MPO) activities, and surface expression of endothelial adhesion molecules was determined using an enzyme immunoassay. RESULTS: High glucose concentrations (over 27.8 mM) increased endothelial-neutrophil cell adhesion and expression of endothelial adhesion molecules (intercellular adhesion molecule-1 (ICAM-1), P-selectin, E-selectin). These events were protein kinase C (PKC) dependent, because PKC inhibitors, but not other intracellular second messenger inhibitors, significantly blocked them. Among antidiabetic medicines, a sulfonylurea, gliclazide (but not glibenclamide or glimepiride), and an aldose reductase inhibitor, epalrestat, significantly inhibited these events; however, a new K(ATP)-channel blocker, netegulinide, a biguanide, metformine, or an insulin sensitizer, troglitazone, did not. CONCLUSIONS: Our data is consistent with hyperglycemia-mediated vascular inflammation through increases in neutrophil adhesion and expression of endothelial adhesion molecules. These events might lead to the onset of atherosclerosis-mediated serious diseases, but could be inhibited by something perhaps, such as gliclazide and epalrestat.
Carbazoles↗
Inhibition of tyrosine kinases blocks adhesion-induced T-cell coactivation without interfering with T-cell adhesion to endothelial cell-surface ligands.
Integrin and cell adhesion molecule-regulated cellular adhesion plays an integral part in the recruitment and activation of lymphocytes. T-cell activation is a dynamic process subject to integrin-dependent and -independent regulation. Stimulation of human peripheral blood T cells by the anti-CD3 monoclonal antibody results in a rapid upregulation of integrin affinity. In conjunction with adhesion to endothelial cell-derived ligands and extracellular matrix proteins, anti-CD3 antibodies have been shown to result in significant increases in IL-2 production and T-cell proliferation. Therefore, at least two signal cascades are activated by ligation of the TCR: One results in a change in affinity of integrins for their ligands, whereas the other activates a signaling cascade that leads to gene induction. We investigated the effects of several tyrosine kinase inhibitors on human peripheral blood T-cell adhesion and adhesion-induced costimulation of IL-2 expression and secretion. These compounds did not inhibit anti-CD3-induced short-term (30 min) or long-term (18 hr) T-cell adhesion to VCAM-1, MAdCAM, or ICAM-1. When T cells were stimulated with anti-CD3 and allowed to adhere to VCAM-1, MAdCAM, or ICAM-1 in the presence of these inhibitors; IL-2 production was significantly reduced. The MEK specific inhibitor, PD98059, did not block T-cell adhesion to the various substrates, but it did block IL-2 synthesis. In addition, the tyrosine kinase inhibitors and PD98059 blocked anti-CD3-mediated stimulation of IL-2 synthesis. These data suggest that the signaling mechanism for anti-CD3-mediated integrin activation is distinct from the signaling pathway that results in adhesion-induced IL-2 synthesis via specific integrins and anti-CD3.
Antibodies, Monoclonal↗
Tannin-bearing hydrogel adhesives with enhanced mechanical and adhesion strength in response to protein leakage.
Anastomotic leaks are among the most severe side effects following abdominal surgeries. Conventional surgical sealants and emerging hydrogel adhesives often lose mechanical and adhesion strength when exposed to leaked digestive enzymes. Here, we report a tannin-encapsulating tough hydrogel adhesive that exhibits enhanced mechanical and adhesive properties upon the encounter of leaked proteins. The hydrogel is composed of a gelatin-acrylate crosslinked network with encapsulated tannin and can adhere to a wet surface via amine-carboxyl chemistry. In the context of anastomotic leaks, tannin within the hydrogel can form a complex with proteins including the digestive enzymes, leading to increased gel stiffness and storage modulus. The enhanced mechanical strength confers improved adhesive properties on the hydrogel adhesive. Additionally, the tannin-bearing hydrogel adhesive shows excellent antibacterial properties. This adaptive and antibacterial hydrogel adhesive provides a promising sealant for gastrointestinal surgery and other applications.
Tannins↗
Endothelial-leukocyte adhesion molecule 1 stimulates the adhesive activity of leukocyte integrin CR3 (CD11b/CD18, Mac-1, alpha m beta 2) on human neutrophils.
Two classes of adhesion molecules have well-defined roles in the attachment of unstimulated polymorphonuclear leukocytes (PMN) to cytokine-treated endothelial cells. Endothelial-leukocyte adhesion molecule 1 (ELAM-1) on endothelial cells interacts with specific carbohydrate residues on the PMN, and the leukocyte integrins (CD18 antigens) on PMN interact with intracellular adhesion molecule 1 and other structures on endothelium. Here we show that these two classes of molecules can act sequentially in an "adhesion cascade". Interaction of PMN with ELAM-1-bearing endothelial cells causes PMN to express enhanced adhesive activity of the integrin CR3 (CD11b/CD18). Expression of ELAM-1 on the cytokine-treated endothelium appears both necessary and sufficient for the stimulation of CR3 activity since blockade of ELAM-1 with mAbs prevents the activation of CR3 by cytokine-treated endothelium, and immobilized recombinant ELAM-1 activates CR3. The ability to activate CR3 is shared by chemattractants, suggesting that ELAM-1 may serve as a "tethered chemattractant." This hypothesis is strengthened by the observation that recombinant soluble ELAM-1 directs movement of PMN in chemotaxis chambers. These results suggest a mechanism by which multiple adhesive molecules may function together in diapedesis. ELAM-1 serves both as an adhesin and as a trigger that recruits the participation of additional adhesion molecules. Our results also suggest that ligands for adhesion molecules may also be "receptors" capable of generating intracellular signals.
Antibodies, Monoclonal↗
Human peripheral blood eosinophils express a functional c-kit receptor for stem cell factor that stimulates very late antigen 4 (VLA-4)-mediated cell adhesion to fibronectin and vascular cell adhesion molecule 1 (VCAM-1).
We evaluated mature peripheral blood eosinophils for their expression of the surface tyrosine kinase, c-kit, the receptor for the stromal cell-derived cytokine, stem cell factor (SCF). Cytofluorographic analysis revealed that c-kit was expressed on the purified peripheral blood eosinophils from 8 of 8 donors (4 nonatopic and 4 atopic) (mean channel fluorescence intensity 2.0- 3. 6-fold, average 2.8 +/- 0.6-fold, greater than the negative control). The uniform and selective expression of c-kit by eosinophils was confirmed by immunohistochemical analysis of peripheral blood buffy coats. The functional integrity of c-kit was demonstrated by the capacity of 100 ng/ml (5 nM) of recombinant human (rh) SCF to increase eosinophil adhesion to 3, 10, and 30 microg/ml of immobilized FN40, a 40-kD chymotryptic fragment of plasma fibronectin, in 15 min by 7.7 +/- 1.4-, 5.3 +/- 3.3-, and 5.4 +/- 0. 2-fold, respectively, and their adhesion to 0.1, 0.5, and 1.0 microg/ml vascular cell adhesion molecule-1 (VCAM-1), by 12.7 +/- 9. 2-, 3.8 +/- 2.5-, and 1.7 +/- 0.6-fold, respectively. The SCF-stimulated adhesion occurred without concomitant changes in surface integrin expression, thereby indicating an avidity-based mechanism. rhSCF (100 ng/ml, 5 nM) was comparable to rh eotaxin (200 ng/ml, 24 nM) in stimulating adhesion. Cell adhesion to FN40 was completely inhibited with antibodies against the alpha4 and beta1 integrin subunits, revealing that the SCF/c-kit adhesion effect was mediated by a single integrin heterodimer, very late antigen 4 (VLA-4). Thus, SCF represents a newly recognized stromal ligand for the activation of eosinophils for VLA-4-mediated adhesion, which could contribute to the exit of these cells from the blood, their tissue localization, and their prominence in inflammatory lesions.
Cell Adhesion↗