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PubMed2006

A six-month clinical study of a self-etching and an etch-and-rinse adhesive applied as recommended and after doubling the number of adhesive coats.

PURPOSE: In an intra-individual comparison, a 6-month randomized, controlled prospective study evaluated the clinical performance of a self-etching and an etch-and-rinse adhesive in noncarious cervical lesions applied as recommended and after doubling the number of adhesive coats. MATERIALS AND METHODS: Twenty-nine patients with at least two pairs of similar sized noncarious cervical lesions participated. One hundred sixteen restorations were placed and divided into the following groups: OS2: phosphoric acid + One Step Plus applied accordingto manufacturer's recommendation (2 coats of adhesive); OS4: phosphoric acid + One Step Plus (4 coats of adhesive); TY2: Tyrian SPE + One Step Plus applied according to manufacturer's recommendation (2 coats of adhesive); TY4: Tyrian SPE + One Step Plus (4 coats of adhesive). The restorations were evaluated at baseline and after 6 months according to the modified USPHS criteria. Statistical analysis was performed with Friedman repeated measures ANOVA by rank and the Wilcoxon sign-ranked test for pairwise significance (alpha = 0.05). RESULTS: One hundred eight restorations were evaluated at 6 months. The retention rate of the group TY2 was statistically significantly lower than the other groups. Marginal discoloration occurred in all groups, being significantly worst in the group TY2. CONCLUSION: Tyrian SPE + One Step Plus applied according to manufacturer's recommendations did not meet the ADA provisional acceptance criteria for enamel-dentin bonded restorative materials. The use of four coats of the One Step Plus in the self-etching approach can improve its clinical performance.

Adhesives↗
PubMed1991

13-Hydroxyoctadecadienoic acid (13-HODE) metabolism and endothelial cell adhesion molecule expression: effect on platelet vessel wall adhesion.

Endothelial cells synthesize two important fatty acid metabolites, PGI2, which is synthesized from arachidonic acid via the cyclooxygenase pathway, and 13-HODE, which is synthesized from linoleic acid via the lipoxygenase pathway. PGI2 is synthesized following cell activation or injury while 13-HODE is synthesized in the unstimulated cell. While the role of PGI2 in platelet vessel wall interactions has been studied extensively, the role of 13-HODE in platelet vessel wall interactions is just now being understood. The present evidence suggests that 13-HODE is continuously synthesized in "resting" vessel wall cells and is in close juxtaposition with the ubiquous integrin adhesion molecule, the vitronectin receptor. The observation that the endothelial cell is not adhesive when 13-HODE and the vitronectin receptor are in close association and becomes adhesive when these two moieties dissociate and the vitronectin receptor relocates on the surface of the cell, provides further evidence that 13-HODE may induce conformational changes in the vitronectin receptor to reduce its ability to recognize its adhesive ligands. The additional observations that 13-HODE levels in both human and animal vessel walls are inversely related with vessel wall adhesivity, and that this adhesivity can be altered by altering 13-HODE synthesis, provides evidence that 13-HODE down-regulates the thrombogenecity of the injured vessel wall surface.

Animals↗
PubMed1989

Role of the LFA-1 adhesion glycoprotein in neutrophil adhesion to endothelium and plastic surfaces.

Neutrophil adherence to endothelium is known to be mediated, at least in part, by adhesion molecules such as LFA-1. Deficiency of these adhesion molecules leads to recurrent infection and early death from infection. As screening for defects of these adhesion glycoproteins is often performed by the ability of neutrophils to adhere to plastic plates, in this study a comparison of neutrophil adherence by the CD18/CD11a (LFA-1) mechanism to endothelium and plastic surfaces was examined. Baseline neutrophil adherence was two-fold higher to plastic than to endothelium (17% +/- 9 for plastic, 8% +/- 5 for endothelium). Baseline adherence to endothelium was partially inhibitable by anti-LFA-1 antibodies, whereas no inhibition of adherence occurred on plastic. Neutrophil stimulants increased adherence to both surfaces, although only on endothelium was this increase attributable to the LFA-1 mechanism. IL-1 increased adherence to endothelium, but had no effect on plastic. We conclude that adherence of neutrophils to plastic surfaces probably represents overall activation status through undefined mechanisms, is not by LFA-1 receptor ligand interactions, and is therefore a non-physiological phenomenon. Endothelial receptors are pivotal in neutrophil adherence. It would be more appropriate to screen leucocytes for leucocyte adhesion deficiency by assaying for specific receptor occupancy with monoclonal antibodies, rather than an assay such as adhesion to plastic where the adhesion ligand is non specific.

Antigens, Differentiation↗
PubMed1989

[A study on the promotion of adhesion properties of adhesives to metals treated by positive oxidation].

The adhesion to three alloys: Durabond, GH30 and soft Co-Cr, by PE adhesive was investigated. The surfaces of metals were treated by polishing, sand-blasting, positive-oxidation and complex processing in order to test the tensile bond strengths between metals and PE adhesive; to study the effects of the surface treatment of metals on adhesive properties; and to compare the tensile strength with that from the control experiment with EB composite resin and Panavia-EX resin under the same conditions. The results showed the mean tensile bond strengths between PE adhesive and Durabond, GH30 and soft Co-Cr alloys after the treatment of sandblasting and positive oxidation were 214.65 +/- 51.68 kg/cm2, 372.88 +/- 21.88 kg/cm2 and 349.21 +/- 48.32 kg/cm2 respectively, displaying better adhesive properties and stability of resistance to water.

Adhesives↗
PubMed1979

[Application of 4-META on adhesive opaque resin. (Part 1) Adhesive strength and the stability (author's transl)].

Mechanical devices, which has been conventionally used for retaining thermo-setting acrylic resin veneers possesses disadvantage of poor marginal sealing and requires rather complicated procedure applying on the metal casting. An application of adhesive resins to overcome these disadvantages was studied. Adhesive opaque resin consisted of MMA, epoxy acrylate, TiO2 and adhesive monomer 4-META was prepared and the adhesive bonding strength between the opaque resin and Ni-Cr alloy which is for crown and bridge works, was measured. As the results, the opaque resin applied on the metal casting with proper surface treatment showed an excellent adhesive bonding strength of 260 kg/cm2. This value did not decreased even after subjected to 300 time thermal cyclings (4 degrees C and 60 degrees C). After a three months immersion in water at 37 degrees C, adhesive bonding strength decreased slightly to 190 kg/cm2.

Acrylic Resins↗
PubMed1979

[Application of 4-META on adhesive opaque resin. (Part 2) Improvement of adhesive stability (author's transl)].

We had reported 4-META adhesive opaque resin for a metal casting etched with HC1. The bonding strength was as excellent as 260 kg/cm2 after 300 times thermal cycles between 4 degrees C and 60 degrees C but it decreased to 70 kg/cm2 when immersed in water at 37 degrees C for 30 weeks. It was required to improve the stability of bonding against water penetration into the adhesive junction before the clinical application. Preparation of the passive state on the metal casting adhesive stability between this film and the opaque resin were studied in this paper. When the metal casting was dipped in conc. HNO3 for fifteen minutes, adhesive strength was 260 kg/cm2 even after a 30 weeks immersion in water at 37 degrees C or the 10 weeks at 80 degrees C. It could be concluded that the adhesive opaque resin possesses enough adhesive strength and the stability for oral application.

Acrylates↗
PubMed1995

[Lymphocyte adhesion of human peripheral blood to aortic endothelial cells of a porcine xenograft: preferential adhesion to NK CD3-CD16+ cells].

Xenotransplantation, the transplantation of tissues or organs between species find renewal interest because of human organ shortage. As the xenogeneic transplantation leads immediately to an humoral mediated rejection with graft necrosis, the study of the cellular response is not possible in vivo. So we developed an in vitro model to study the adhesion of human peripheral blood lymphocytes (PBL) to porcine aortic endothelial cells (PAEC). We showed that PBL were able to bind to PAEC, and that this adhesion was increased when PAEC were stimulated with human recombinant TNF-alpha. The action of TNF-alpha is maximal when PAEC were stimulated during 6 hours with 100 U/ml TNF-alpha. This adhesion involved preferentially CD3-CD16+ NK cells compared with CD3+CD16- T lymphocytes. Finally monoclonal antibodies directed against PBL adhesion molecules decreased PBL adhesion to PAEC. PBL adhesion to PAEC would be a first step in a cellular mediated rejection in xenotransplantation.

Animals↗
PubMed1996

Utilization of the serosal scarification model of postoperative intestinal adhesion formation to investigate potential adhesion-preventing substances in the rabbit.

A rabbit serosal scarification model was utilized to compare the ability of four drugs, previously administered peri-operatively to horses undergoing exploratory celiotomy, to prevent the development of postoperative intestinal adhesions. The substances compared were 32% Dextran 70 (7 mL/kg), 1% sodium carboxymethylcellulose (7 mL/kg), trimethoprim-sulfadiazine (30 mg/kg), and flunixin meglumine (1 mg/kg). The first two were administered intra-abdominally following surgery, while the latter two were administered systemically in the peri-operative period. Fibrous adhesions were evident in all animals in the untreated serosal scarification group. No significant difference in the number of animals with adhesions was found between the untreated control group and any treatment group, nor among the treatment groups. Microscopic examination of adhesions collected at postmortem examination revealed fibers consistent with cotton, surrounded by a giant-cell reaction and ongoing acute inflammation. The source of the fibers was likely the cotton laparotomy sponges used to scarify the intestinal surface, since the pattern in the granuloma and sponge fibers appeared similar under polarized light. Though consistent intestinal adhesion formation was produced in the rabbit, the presence of foreign body granulomas may prevent consideration of this model for future research. The drugs tested were ineffective in preventing the formation of postoperative small intestinal adhesions in this model.

Animals↗
PubMed1996

Reduction of adhesions after uterine myomectomy by Seprafilm membrane (HAL-F): a blinded, prospective, randomized, multicenter clinical study. Seprafilm Adhesion Study Group.

OBJECTIVE: To assess the safety and efficacy of Seprafilm (HAL-F), Bioresorbable Membrane, (Genzyme Corporation, Cambridge, MA) in reducing the incidence, severity, extent, and area of uterine adhesions after myomectomy. DESIGN: Prospective, randomized, blinded, multicenter study. Adhesion reduction was assessed by an independent, blinded, gynecologic surgeon who reviewed videotapes of each patient's second-look laparoscopy. SETTING: Nineteen institutions across the United States. PATIENT(S): One hundred twenty-seven women undergoing uterine myomectomy with at least one posterior uterine incision > or = 1 cm in length. INTERVENTION(S): Patients were randomized to treatment with Seprafilm or to no treatment at the completion of the myomectomy. MAIN OUTCOME MEASURE(S): The incidence, severity, extent, and area of uterine adhesions at second-look laparoscopy. RESULT(S): The incidence, measured as the mean number of sites adherent to the uterine surface, was significantly less in treated patients (4.98 +/- 0.52 [mean +/- SEM] sites) than in no treatment patients (7.88 +/- 0.48 sites) as were the mean uterine adhesion severity scores (1.94 +/- 0.14 versus 2.43 +/- 0.10; treatment versus no treatment, respectively), mean extent scores (1.23 +/- 0.12 versus 1.68 +/- 0.10), and mean area of adhesions (13.2 +/- 1.67 versus 18.7 +/- 1.66 cm2). No adverse events occurred that were judged to be related to the use of Seprafilm. CONCLUSION(S): In this multicenter study, treatment of patients after myomectomy with Seprafilm significantly reduced the incidence, severity, extent, and area of postoperative uterine adhesions. Additionally, Seprafilm treatment was not associated with an increase in postoperative complications.

Adult↗
PubMed2000

Specific decrease in the level of Hic-5, a focal adhesion protein, during immortalization of mouse embryonic fibroblasts, and its association with focal adhesion kinase.

Hic-5 is a paxillin homologue with four LIM domains in its C-terminal region, localized mainly in focal adhesions in normal fibroblasts. Hic-5 is also known to associate with focal adhesion kinase (FAK) or the related CAKbeta, and with vinculin. In the present study, we examined changes in Hic-5 and paxillin protein levels in primary mouse embryo fibroblasts (MEF) during mortal and immortal stages. The Hic-5 level was markedly decreased when cells became immortalized, whereas that of paxillin was increased. The vinculin level was not changed significantly. Hic-5 was mainly localized in focal adhesion plaques of mortal MEF but was localized in the nuclear periphery in the immortalized MEF; the number of focal adhesion plaques was decreased in these cells. Mouse Hic-5 contains three LD domains in its N-terminal half, and the first LD domain (LD1) appears to be involved in interaction with FAK. However, this interaction was not essential for recruitment of Hic-5 to focal adhesions, since its subcellular localization was similar in FAK(-/-) cells. Forced expression of Hic-5 decreased colony forming ability of MEF from FAK(+/+) mice, but not of FAK(-/-) cells. These observations suggested the involvement of Hic-5 in determination of cellular proliferative capacity in collaboration with other cytoskeletal components.

Amino Acid Sequence↗
PubMed1993

Circulating intercellular adhesion molecule-1 levels and neutrophil adhesion in stroke.

To examine whether changes in leukocyte adhesion properties occur during stroke, we measured circulating serum intercellular adhesion molecule 1 (cICAM-1) levels and neutrophil adhesion in acute stroke, patients at high risk of stroke, and in matched controls. Levels of cICAM-1 were significantly lower in the stroke group (186.2 +/- 15.6 ng ml-1) compared to controls (257.7 +/- 24.8) and risks (257.7 +/- 16.5). Neutrophil adhesion was significantly higher in the stroke group (23.6 +/- 4.3%; n = 14) compared to controls (9.7 +/- 2.3%; n = 12) and risks (12.7 +/- 2.5%; n = 13). These data suggest that changes in leukocyte adhesion dynamics are occurring in acute stroke.

Cell Adhesion↗
PubMed2006

Protection from procedural myocardial injury by atorvastatin is associated with lower levels of adhesion molecules after percutaneous coronary intervention: results from the ARMYDA-CAMs (Atorvastatin for Reduction of MYocardial Damage during Angioplasty-Cell Adhesion Molecules) substudy.

OBJECTIVES: The goal of this work was to investigate whether protection from myocardial injury during percutaneous coronary intervention (PCI) by atorvastatin is related to reduction of endothelial inflammatory response. BACKGROUND: In the randomized ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) trial, 7-day pre-treatment with atorvastatin before PCI significantly reduced procedural myocardial injury; mechanisms underlying this effect are not characterized. METHODS: In a planned subanalysis of the ARMYDA trial, a subgroup of 76 patients was blind-tested for measurement of plasma levels of vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), and E-selectin: 38 patients belonged to atorvastatin (40 mg/day) and 38 to the placebo arm. Adhesion molecules were evaluated 7 days before intervention, immediately before PCI, and after 8 and 24 h. RESULTS: Reduction of procedural myocardial injury after statin pre-treatment was also confirmed in this subgroup. Intercellular cell adhesion molecule-1, E-selectin, and VCAM-1 levels were not different at randomization and before intervention in either arm. At 8 h, increase of ICAM-1 levels was similar in the 2 arms, whereas 24-h levels were significantly lower in the atorvastatin versus placebo group (282 +/- 56 vs. 325 +/- 70 ng/ml; p = 0.007). Attenuation of E-selectin elevation occurred at 8 h in the atorvastatin group (50 +/- 8 vs. 59 +/- 13 ng/ml; p = 0.002) and became even more significant at 24 h (57 +/- 9 vs. 73 +/- 18 ng/ml; p = 0.0008). Vascular cell adhesion molecule-1 levels were not different at any time point in the 2 arms. CONCLUSIONS: In patients undergoing PCI, reduction of procedural myocardial injury after 7-day pre-treatment with atorvastatin is paralleled by concomitant attenuation of post-procedural increase of ICAM-1 and E-selectin levels; thus, reduction of endothelial inflammatory response may explain this protective effect of statins.

Angina Pectoris↗
PubMed2005

Insulin enhances leukocyte-endothelial cell adhesion in the retinal microcirculation through surface expression of intercellular adhesion molecule-1.

The purpose of this study was to evaluate the effects of insulin on leukocyte-endothelial cell adhesion in the retinal microcirculation in vitro and in vivo. Human retinal endothelial cells (HRECs) were cultured in medium with or without insulin, and neutrophils allowed to adhere. Adherent neutrophils were quantified by measuring myeloperoxidase activity. Surface expression of endothelial adhesion molecules were studied with the use of an enzyme immunoassay. Insulin at concentrations of 50 and 100 microU/ml significantly increased neutrophil adhesion to HRECs compared with the control cells (P < 0.01, respectively). Surface expression of intercellular adhesion molecule-1 (ICAM-1) significantly increased when HRECs were exposed to 100 microU/ml insulin, as compared with the control cells (P < 0.05). Anti-ICAM-1 antibody significantly inhibited neutrophils adhesion to HRECs (P < 0.0001). Brown-Norway rats received subcutaneous injection of 0.2 U per 100 g body weight insulin three times. Control rats received the same amount of phosphate-buffered saline. Leukocyte entrapment in the retina was evaluated using acridine orange leukocyte fluorography. The number of leukocytes trapped in the retina of insulin-treated rats was significantly elevated compared with that in the control animals (P < 0.0001). These results suggested that insulin enhances leukostasis in retinal microcirculation. Hyperinsulinemia may be a risk factor of retinal microcirculatory disturbances.

Acridine Orange↗
PubMed2002

Stimulation of adhesion molecule expression by Helicobacter pylori and increased neutrophil adhesion to human umbilical vein endothelial cells.

Helicobacter pylori upregulates endothelial adhesion molecules but the pattern is unclear. Human umbilical vein endothelial cells (HUVEC) were exposed to control medium or H. pylori 60190. Binding of monoclonal antibodies against P-selectin, E-selectin, vascular adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) was determined using enzyme-linked immunosorbent assay. Binding of polymorphonuclear leukocytes to HUVEC was determined on cells exposed as above. After 6 h exposure to H. pylori, there were 30%, 124%, 167% and 100% increases in P-selectin, E-selectin, VCAM-1 and ICAM-1 levels and a 400% increase in polymorphonuclear leukocyte adhesion in HUVEC exposed to H. pylori. Effects of incubation for other intervals between 0 and 18 h are also described. H. pylori exerts some of its effects on gastric mucosa via gastric vasculature. This study gives insight into the pattern of H. pylori-associated endothelial adhesion molecule upregulation.

Cell Adhesion↗
PubMed2000

Interferon-gamma up-regulates intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 and recruits lymphocytes into the vagina of immune mice challenged with herpes simplex virus-2.

Lymphocyte recruitment into tissues involves interactions between adhesion molecules on vascular endothelial cells and corresponding ligands on the lymphocyte surface. In the present study we investigated the expression of four endothelial addressins in the vagina and their possible up-regulation by interferon-gamma (IFN-gamma) in immune mice after vaginal challenge with herpes simplex virus type 2. The adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were minimally expressed in the vagina of non-immune mice with or without vaginal challenge and in immune mice before challenge, but both were up-regulated by IFN-gamma, directly or indirectly, in immune mice after challenge. Mucosal addressin cell adhesion molecule-1 (MAdCAM-1) was detected in most vaginas but was not up-regulated by IFN-gamma in immune mice after virus challenge. E-selectin was not detected in any vaginas. The results suggest that ICAM-1 and VCAM-1 may be involved in rapid, IFN-gamma-mediated recruitment of lymphocytes to the vaginal mucosal of immune mice after local virus challenge.

Animals↗
PubMed1996

p130Cas, a substrate associated with v-Src and v-Crk, localizes to focal adhesions and binds to focal adhesion kinase.

p130(Cas) (crk associated substrate) has the structural characteristics of an adapter protein, containing multiple consensus SH2 binding sites, an SH3 domain, and a proline-rich domain. The structure of p130(Cas) suggests that it may act to provide a framework for protein-protein interactions; however, as yet, its functional role in cells is unknown. In this report we show that p130(Cas) is localized to focal adhesions. We demonstrate that p130(Cas) associates both in vitro and in vivo with pp125(FAK) (focal adhesion kinase), a kinase implicated in signaling by the integrin family of cell adhesion receptors. p130(Cas) also associates with pp41/43(FRNK) (pp125(FAK)-related, non-kinase), an autonomously expressed form of pp125(FAK) composed of only the C-terminal noncatalytic domain. We show that the association of p130(Cas) with pp125(Fak) and pp41/43(FRNK) is direct, and is mediated by the binding of the SH3 domain of p130(Cas) to a proline-rich sequence present in both the C terminus of pp125(FAK) and in pp41/43(FRNK). In agreement with recent studies we show that p130(Cas) is tyrosine-phosphorylated upon integrin mediated cell adhesion. The association of p130(Cas) with pp125(FAK), a kinase which is activated upon cell adhesion, is likely to be functionally important in integrin mediated signal transduction.

Animals↗
PubMed1998

Lactosylceramide mediates tumor necrosis factor-alpha-induced intercellular adhesion molecule-1 (ICAM-1) expression and the adhesion of neutrophil in human umbilical vein endothelial cells.

The endothelial expression of adhesion molecules by proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) has been suggested to contribute to the initiation of atherosclerotic plaque formation. Since lactosylceramide (LacCer) accumulates in large quantities in human atherosclerotic plaque, we have explored its role in TNF-alpha-induced expression of intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells and their consequent adhesion to polymorphonuclear leukocytes (PMNs). We found that TNF-alpha increased LacCer synthesis by way of stimulating the activity of UDP-galactose:glucosylceramide beta(1-->4)-galactosyltransferase in a time-dependent fashion. The TNF-alpha-induced expression of ICAM-1 was abrogated by D-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of UDP-galactose:glucosylceramide beta(1-->4)-galactosyltransferase. However, the addition of LacCer reversed the D-PDMP effect on TNF-alpha-induced ICAM-1 expression in human umbilical vein endothelial cells. Northern hybridization analysis of mRNA levels and enzyme-linked immunosorbent assays revealed that LacCer (5 microM) specifically stimulated ICAM-1 at both the transcriptional and translational levels. This was accompanied by the adhesion of PMNs, which was visualized by confocal microscopy. Further studies revealed that LacCer stimulated the endogenous generation of superoxide radicals (O-2) about 5-fold compared with the control by specifically activating plasma membrane-associated NADPH-dependent oxidase. This phenomenon was blocked by the antioxidant N-acetyl-L-cysteine, pyrrolidine dithiocarbamate, and the NADPH oxidase inhibitor, diphenylene iodonium. Overexpression of endogeneous CuZn-superoxide dismutase via an adenoviral vector carrying cDNA for CuZn-superoxide dismutase, also inhibited LacCer-induced ICAM-1 expression in endothelial cells. In sum, our findings suggest that LacCer may play the role of a lipid second messenger in TNF-alpha-induced pathogenesis by activating an oxidant-sensitive transcriptional pathway that leads to the adhesion of PMNs to endothelial cells.

Antigens, CD↗
PubMed2004

Sodium arsenite exposure alters cell migration, focal adhesion localization and decreases tyrosine phosphorylation of focal adhesion kinase in H9C2 myoblasts.

Exposure to the environmental toxicant arsenic is reported to produce a variety of effects including disruption of signal transduction pathways, cell proliferation, and apoptosis. This suggests that arsenite may not have specific targets but rather extremely broad effects. The present study was designed to test the hypothesis that arsenite alters signaling involved in focal adhesion structure and function in cultured myoblasts. H9C2 cells were exposed to 1, 2.5, 5, or 10 microM sodium arsenite for 48 h. MTT metabolism and staining by neutral red, trypan blue, and propidium iodide showed that sodium arsenite treatments of 5 microM or less were not overtly cytotoxic. At these doses, sodium arsenite did not affect the amount of polymerized actin in cells, rate of protein synthesis, or amounts of vinculin, talin, paxillin, and focal adhesion kinase (FAK) in cells. However, sodium arsenite-treated cells contained fewer focal adhesions with an altered distribution pattern. Sodium arsenite exposure caused a dose-dependent reduction in cell migration and cell attachment rates. The average area of substrate covered by a cell was also reduced, although the average volume of cells was not significantly affected. Sodium arsenite exposure resulted in reduced tyrosine phosphorylation of FAK, its substrate paxillin and the FAK auto- phosphorylation site, Tyr397. Our results indicate that sodium arsenite can alter focal adhesion structure and function, thus affecting cell attachment and migration and possibly other aspects of focal adhesion function such as integrin signaling. These diverse consequences may be mediated by a relatively specific inhibition of FAK tyrosine phosphorylation, modifying scaffolding proteins.

Animals↗