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PubMed1996

Matrix-specific effect of endothelial control of smooth muscle cell migration.

PURPOSE: Smooth muscle cell (SMC) migration is a critical element in the development of intimal hyperplasia. The effect of endothelial cells (ECs) on SMC migration and the modulation of this cell-to-cell interaction by extracellular matrix is not well understood. METHODS: To examine this relationship SMCs and ECs were cocultured on opposite sides of a semipermeable membrane and were compared with SMCs cultured alone. To assess migration SMCs were plated at confluent density into the center of the membrane with a steel fence. After the fence was removed, SMCs were treated for 2 hours with mitomycin C (20 micrograms/ml) to assess migration independent of proliferation. Cell migration was measured with morphometry. Experiments were performed on plastic and membranes coated with fibronectin or type I collagen (n > or = 8/group). Cell adhesiveness was quantitated by cell attachment and spreading assays. RESULTS: ECs stimulated SMC migration by 187% when compared with SMCs cultured alone on plastic and by 160% when cultured on fibronectin (p < 0.01). Type I collagen stimulated migration of SMCs cultured alone and prevented EC stimulated migration in cocultured SMCs (p < 0.01). Cell adhesiveness was significantly increased in cocultured SMCs compared with SMCs cultured alone regardless of whether cells were cultured on plastic (EC/SMC, 13.5 +/- 0.6 SMCs/high power field vs SMC, 8.9 +/- 0.5, p < 0.01), fibronectin (16.3 +/- 0.8 vs 12.3 +/- 0.7, p < 0.01) or type I collagen (15.5 +/- 1.0 vs 12.4 +/- 0.6, p < 0.01). ECs increased SMC cell spreading on plastic and fibronectin when compared with SMCs cultured alone. No difference in SMC cell spreading was seen in the presence or absence of ECs when cells were cultured on type I collagen. EC-SMC contact was not required; EC-conditioned media alone increased SMC migration by 75% when compared with SMCs cultured alone. Our data suggest that ECs increase SMC migration by a diffusable molecule that may also alter SMC adhesion molecule expression. Extracellular matrix composition can attenuate these effects.

Animals↗
PubMed1996

Docosapentaenoic acid (22:5, n-3), an elongation metabolite of eicosapentaenoic acid (20:5, n-3), is a potent stimulator of endothelial cell migration on pretreatment in vitro.

Endothelial cell (EC) migration plays an important role in wound repair of blood vessels. We have previously reported that eicosapentaenoic acid (EPA; 20:5, n-3) pretreatment stimulates migration of ECs but not smooth muscle cells. In the present study, we used the modified Boyden chamber technique to investigate whether the stimulative effect of EPA pretreatment on EC migration is caused by EPA itself or by some metabolites of EPA. When ECs were treated with EPA (5 micrograms/ml) for 2 days, EPA was predominantly elongated to docosapentaenoic acid (DPA; 22:5, n-3), with little docosahexaenoic acid (DHA; 22:6, n-3) being formed. Direct pretreatment of ECs with DPA (0.01-1.0 microgram/ml) resulted in a dose-dependent increase in migration in response to fetal bovine serum. Moreover, maximum stimulation of EC migration by DPA pretreatment (0.5 microgram/ml) was achieved at a concentration one-tenth of that required for maximal stimulation by EPA pretreatment (5.0 micrograms/ml), indicating that DPA is a potent stimulator of EC migration. We have demonstrated by lipid analysis that direct DPA pretreatment (0.5 microgram/ml) sufficiently increased the absolute quantity of phospholipids of ECs. Cyclooxygenase inhibitor and lipoxygenase inhibitor did not abolish the stimulative effect of DPA pretreatment on EC migration. In contrast to EC migration, DPA pretreatment had no effect on smooth muscle cell migration. Together these data suggest that the stimulative effect of EPA on EC migration occurs via DPA, and that DPA may act as a powerful anti-atherogenic factor.

Animals↗
PubMed2002

Effect of geographic migration on SMI prevalence estimates.

The prevalence of serious mental illness (SMI) varies by the socioeconomic characteristics of communities. This variation is presumed to be due to the differential incidence of disorders caused by adverse social factors (social causation) and differential geographic migration (social selection and drift). The objective of this study was to measure the geographic migration patterns of adults treated for SMI. A sample of 11,725 adults with three or more psychiatric hospital admissions between July 1978 and November 1992 was drawn from inpatient records. At least one third migrated to different counties between first and last admission. Migration rates were higher for Whites than for African Americans and higher for unmarried than for married patients. There were no significant differences in migration rates by gender or mental disorder. Patient migration did not parallel shifts in the general population. Patient migration was generally toward medium-size, low-income urban counties with relatively declining general populations, and movement was away from both the most rural and the largest urban counties. Public needs assessments and resource allocation policies may understate the need in communities with net SMI out-migration and overstate endemic need where there is net in-migration. In the long term, these same policies may induce migration through resource allocation decisions.

Adolescent↗
PubMed2001

Migration of osteoblastic cells on various guided bone regeneration membranes.

To evaluate the biological effects of guided bone regeneration (GBR) barrier materials on osteoblastic cell migration, migration of mouse osteoprogenitor cells (MC3T3-E1) was examined, in vitro, on various membranes. Eight commercially available GBR membranes - bovine type I collagen (BioMend; BM), porcine type I collagen (BioGide; BG), bovine type I atelocollagen (Tissue Guide; TG), polylactic acid (Epi-Guide; EG), co-polymer of polylactic acid and polyglycolic acid (Resolute; RL, Resolut XT; RL-XT), expanded polytetrafluoroethylene (e-PTFE; Gore Tex; GT) and co-polymer of cellulose acetate and nitrocellulose (Millipore filter; MP) - were tested. A 3x5 mm section of the membrane was fixed to the bottom of a culture dish with double-sided adhesive tape, and half of the membrane was closely covered by PARAFILM (American National Can) to leave an unexposed area for cell migration. The border between exposed and unexposed areas was marked as a baseline of cell migration. Membranes were then plated with 3 ml of cell suspension at an initial density of 1x105 cells/ml in alpha-MEM culture medium with 10% fetal bovine serum and ascorbic acid. After a 5-hour incubation, non-attached cells were completely washed out with phosphate buffered saline and the PARAFILM cover was removed. After 3 days cultivation, specimens were fixed with 10% buffered formalin and stained briefly with hematoxylin. The area of cell migration on a membrane was analyzed using a LA 500 Image Analysis System and migration area per unit length of the baseline (mm2/mm) was compared among membranes. Results demonstrated that cell migration was greater in the order: RL>RL-XT, BM, TG, MP>EG, BG. Membranes except for BG, EG and GT showed the migration rate equal to or higher than a plastic culture cover slip (Celldesk) (P<0.01) on which cells generally grow favorably. Only a small number of the cells attached to GT, and the net cell migration for the membrane could not be determined. These results indicate that GBR barrier materials per se may influence the process of bone regeneration in vivo through the effects of their presence on cell migration.

Animals↗
PubMed2003

Effect of a kinin B2 receptor antagonist on LPS- and cytokine-induced neutrophil migration in rats.

1 This study examines the involvement of kinins in neutrophil migration into rat subcutaneous air pouches triggered by lipopolysaccharide (LPS), as well as the putative roles played by kinin B(1) and B(2) receptors, tumour necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1beta) and selectins in this response. 2 LPS (5 ng to 10 micro g cavity(-1)) injected into the 6-day-old pouch induced a dose- and time-dependent neutrophil migration which peaked between 4 and 6 h, and was maximal following the dose of 100 ng cavity(-1) (saline: 0.46+/-0.1; LPS: 43+/-3.70 x 10(6) cells cavity(-1) at 6 h). 3 Bradykinin (BK) (600 nmol) injected into the pouch of saline-treated rats induced only modest neutrophil migration (0.73+/-0.16 x 10(6) cells cavity(-1)). A more robust response to BK (3.2+/-0.25 x 10(6) cells cavity(-1)) was seen in animals pretreated with captopril, but this was still smaller than the responses to IL-1beta or TNF-alpha (15 pmol: 23+/-2.2 x 10(6) and 75 pmol: 29.5+/-2 x 10(6) cells cavity(-1), respectively). Nevertheless, the B(1) agonist des-Arg(9)-BK (600 nmol) failed to induce neutrophil migration. 4 HOE-140 (1 and 2 mg kg(-1)), a B(2) receptor antagonist, reduced LPS-induced neutrophil migration. HOE-140 also reduced the neutrophil migration induced by BK, but had no effect on the migration promoted by IL-1beta or TNF-alpha. des-Arg(9)-[Leu(8)]-BK, B(1) receptor antagonist was ineffective in changing neutrophil migration caused by any of these stimuli. 5 Neutrophil migration induced by LPS or BK was reduced by interleukin-1 receptor antagonist (IL-1ra) (1 mg kg(-1)), sheep anti-rat TNF serum (anti-TNF serum) (0.3 ml cavity(-1)), and the nonspecific selectin inhibitor fucoidin (10 mg kg(-1)). 6 TNF-alpha levels in the pouch fluid were increased by LPS or BK injection, peaking at 0.5-1 h and gradually declining thereafter up to 6 h. IL-1beta levels increased steadily throughout the 6 h period. HOE-140 markedly inhibited the rise in IL-1beta and TNF-alpha levels in pouch fluid triggered by both stimuli. 7 These results indicate that BK participates importantly in selectin-dependent neutrophil migration into the air pouch triggered by LPS in the rat, by stimulating B(2) receptors coupled to synthesis/release of TNF-alpha and IL-1beta.

Animals↗
PubMed2006

Interleukin-18 is a critical factor for vascular endothelial growth factor-enhanced migration in human gastric cancer cell lines.

Cell migration and angiogenesis are key steps in tumor metastasis. However, the mechanism of migration regulated by vascular endothelial growth factor (VEGF), a potent regulator of angiogenesis, is not completely understood. This study examined the relationship between VEGF and migration, along with the mechanism involved in the VEGF-regulated migration of human gastric cancer cells. The level of cell migration was increased by recombinant human (rh)VEGF-165 in the VEGF receptor-2-expressing SNU-601 cells. Interleukin (IL)-18 is associated with the malignant progression of tumors. Accordingly, this study examined the effect of IL-18 on the migration of cancer cells in order to identify the factors involved in VEGF-enhanced migration. Inhibiting IL-18 markedly reduced the level of VEGF-enhanced migration, and IL-18 increased cell migration directly through filamentous-actin polymerization and tensin downregulation. It was confirmed that rhVEGF-165 increased IL-18 production significantly. An antioxidant and an extracellular signal-regulated kinase (ERK)1/2-specific inhibitor blocked rhVEGF-165-enhanced IL-18 production. Accordingly, rhVEGF-165 increased the generation of region of interest (ROI) and activated the ERK1/2 pathway. These results suggest that rhVEGF-165 enhances IL-18 production via the generation of ROI and ERK1/2 phosphorylation, which results in the increased migration of gastric cancer cells.

Actins↗
PubMed2003

Proteolytic and non-proteolytic migration of tumour cells and leucocytes.

The migration of different cell types, such as leucocytes and tumour cells, involves cellular strategies to overcome the physical resistance of three-dimensional tissue networks, including proteolytic degradation of extracellular matrix (ECM) components. High-resolution live-cell imaging techniques have recently provided structural and biochemical insight into the differential use of matrix-degrading enzymes in the migration processes of different cell types within the three-dimensional ECM. Proteolytic migration is achieved by slow-moving cells, such as fibroblasts and mesenchymally moving tumour cells, by engaging matrix metalloproteinases, cathepsins and serine proteases at the cell surface in a focalized manner ('pericellular proteolysis'), while adhesion and migratory traction are provided by integrins. Pericellular breakdown of ECM components generates localized matrix defects and remodelling along migration tracks. In contrast with tumour cells, constitutive non-proteolytic migration is used by rapidly moving T lymphocytes. This migration type does not generate proteolytic matrix remodelling, but rather depends on shape change to allow cells to glide and squeeze through gaps and trails present in connective tissues. In addition, constitutive proteolytic migration can be converted into non-proteolytic movement by protease inhibitors. After the simultaneous inhibition of matrix metalloproteinases, serine/threonine proteases and cysteine proteases in tumour cells undergoing proteolysis-dependent movement, a fundamental adaptation towards amoeboid movement is able to sustain non-proteolytic migration in these tumour cells (the mesenchymal-amoeboid transition). Instead of using proteases for matrix degradation, the tumour cells use leucoyte-like strategies of shape change and squeezing through matrix gaps along tissue scaffolds. The diversity of protease function in cell migration by different cell types highlights response diversity and molecular adaptation of cell migration upon pharmacotherapeutic protease inhibitor treatment.

Cell Movement↗
PubMed2002

Matrix metalloproteinases in tumor invasion: role for cell migration.

Matrix metalloproteinases (MMP) play a role in a wide range of tumorigenesis, including early carcinogenesis events, tumor growth and tumor invasion and metastasis. Given that the ability of tumor cells to infiltrate and disseminate widely is what makes the tumors malignant, a role of MMP in cell migration during this invasive and metastatic process is important. There are two types of cancer cell migration: single cell locomotion and cohort migration (cell movement en mass keeping cell-cell contact, which is frequently seen in better differentiated carcinomas). Cell surface localization and activation of MMP is essential for cells to migrate, through rearrangement of extracellular matrix (ECM) to suit cell migration. Certain MMP, such as gelatinases and membrane -type 1 MMP, have special mechanisms to localize at leading edges in both types of cell migration. Moreover, in cohort migration, expression of these MMP is regulated via cell-cell contact within migrating cell sheets and confined to the foremost pathfinder cells of the migrating cell sheets. New roles of cell surface MMP, such as cleavage of cell surface receptors or cofactors involved in cell-ECM interactions during cell migration, are also discussed.

Cell Movement↗
PubMed2003

Involvement of platelet-activating factor and LIS1 in neuronal migration.

Platelet-activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) is a biologically active lipid mediator. We have previously shown the expression of PAF receptor in neurons and microglia. PAF is produced in the brain from its precursor, and degraded by the enzyme PAF acetylhydrolase. LIS1 is a regulatory subunit of PAF acetylhydrolase, and is identical to a gene whose deletion causes the human neuronal migration disorder, type I lissencephaly. Indeed, Lis1 mutant mice display defects in neuronal migration and layering in vivo, and also in cerebellar granule cell migration in vitro. However, the roles of PAF and the PAF receptor in the neuronal migration remain to be determined. Here, we show that PAF receptor-deficient mice exhibited histological abnormalities in the embryonic cerebellum. PAF receptor-deficient cerebellar granule neurons migrated more slowly in vitro than wild-type neurons, consistent with the observation that a PAF receptor antagonist reduced the migration of wild-type neurons in vitro. Synergistic reduction of neuronal migration was observed in a double mutant of PAF receptor and LIS1. Unexpectedly, PAF affected the migration of PAF receptor-deficient neurons, suggesting a receptor-independent pathway for PAF action. The PAF receptor-independent response to PAF was abolished in granule neurons derived from the double mutant mice. Thus, our results suggest that the migration of cerebellar granule cells is regulated by PAF through receptor-dependent and receptor-independent pathways, and that LIS1 is a pivotal molecule that links PAF action and neuronal cell migration both in vivo and in vitro.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2001

Wound-induced migration of rat hepatic stellate cells is modulated by endothelin-1 through rho-kinase-mediated alterations in the acto-myosin cytoskeleton.

Although migration of stellate cells during hepatic injury is essential for wound-healing and fibrosis of the liver, the extracellular and intracellular signals that regulate stellate cell migration are incompletely understood. In this study we tested the hypothesis that wound-induced migration of stellate cells is modulated by endothelin-1 (ET-1) through rho-kinase-mediated alterations in the acto-myosin cytoskeleton. To address this hypothesis, a method was established for direct visualization of wound-induced migration of culture-activated stellate cells with subcellular resolution. Migration in response to wounding was characterized by (1) plasma membrane ruffling and protrusion into the wound, (2) lamellipodia formation at the leading edge, (3) focal adhesion and stress fiber assembly, and (4) myosin reorganization. Exogenous ET-1 accelerated wound-induced migration of stellate cells, but did not alter wound-induced proliferation. Experiments using ET-1 antagonists in the absence of exogenous ET-1 showed that wound-induced migration was also stimulated by endogenous ET-1. Selective inhibition of rho-associated kinase decelerated migration in response to wounding. Moreover, inhibition of rho-associated kinase was distinguished by abrogation of focal adhesion formation, stress fiber assembly, and myosin reorganization. This study shows that rho-kinase-dependent alterations in the acto-myosin cytoskeleton contribute to wound-induced stellate cell migration, which is accelerated by both exogenous and endogenous ET-1. Consequently, these results provide important new evidence suggesting that, migration of stellate cells is modulated by paracrine and autocrine ET-1 stimulation via the action of rho-kinase on the acto-myosin cytoskeleton.

Actomyosin↗
PubMed1994

The kinetics of spontaneous DNA branch migration.

An important step in genetic recombination is DNA branch migration, the movement of the Holliday junction or exchange point between two homologous duplex DNAs. We have determined kinetic parameters of spontaneous branch migration as a function of temperature and ionic conditions. The branch migration substrates consist of two homologous duplex DNAs each having two single-strand tails at one end that are complementary to the corresponding single-strand tails of the other duplex. Upon rapid annealing of the two duplex DNAs, a four-stranded intermediate is formed that has a Holliday junction at one end of the duplexes. Branch migration to the opposite end of the duplexes results in complete strand exchange and formation of two duplex products. The rate of branch migration is exceedingly sensitive to the type of metal ions present. In magnesium, branch migration is quite slow with a step time, tau, equal to 300 msec at 37 degrees C. Surprisingly, branch migration in the absence of magnesium was 1000 times faster. Despite this difference in rates, apparent activation energies for the branch migration step in the presence and absence of magnesium are similar. Since metal ions have a profound effect on the structure of the Holliday junction, it appears that the structure of the branch point plays a key role in determining the rate of spontaneous DNA branch migration. We discuss the role of proteins in promoting the branch migration step during homologous recombination.

Base Sequence↗
PubMed1999

c-Raf-mediated inhibition of epidermal growth factor-stimulated cell migration.

Epidermal growth factor stimulates migration of a number of cell types, yet the signaling pathways that regulate epidermal growth factor-stimulated migration are poorly defined. In this report, we employ a transient transfection migration assay to assess the role of components of the Ras-mitogen-activated protein (MAP) kinase signaling pathway in epidermal growth factor-stimulated chemotaxis of rat embryo fibroblasts. Expression of dominant negative Ras blocks epidermal growth factor-mediated chemotaxis, while constitutively active Ras has no effect on chemokinesis or chemotaxis. PD98059 and U0126, inhibitors of MAP kinase kinase (MEK) activity, decreased epidermal growth factor-stimulated migration, while kinase-defective MEK1, an inhibitor of MAP kinase activation, enhanced migration. To understand the paradoxical effects of these molecules on epidermal growth factor-induced migration, we examined the role of c-Raf on migration. Expression of either wild type c-Raf or the catalytic domain of c-Raf effectively inhibited epidermal growth factor-stimulated cell migration. We suggest that, whereas Ras activity is necessary to promote epidermal growth factor-stimulated migration, sustained activation of c-Raf may be important in down-regulating migratory signaling pathways triggered by epidermal growth factor receptor activation. Further, activation of c-Raf upon inhibition of the MEK-MAP kinase pathway may contribute to the inhibition of cell migration observed with pharmacological MEK inhibitors.

Animals↗
PubMed1999

The adapter protein Crkl links Cbl to C3G after integrin ligation and enhances cell migration.

Crkl, an SH2-SH3-SH3 adapter protein, is one of the major tyrosine phosphoproteins detected in cells from patients with chronic myelogenous leukemia. Crkl binds to BCR/ABL through its N-terminal SH3 domain and is known to interact with several signaling proteins that have been implicated in integrin signaling, including Cbl, Cas, Hef-1, and paxillin. We have previously shown that overexpression of Crkl enhances adhesion to extracellular matrix proteins through beta(1) integrins. In this study, the effects of Crkl on spontaneous and chemokine-directed migration of the hematopoietic cell line Ba/F3 were examined. Full-length, SH2-, and SH3(N)-domain deletion mutants of Crkl were expressed transiently as fusion proteins with green fluorescent protein. Successfully transfected cells were isolated by fluorescence-activated cell sorting. The ability of these cells to migrate across a fibronectin-coated membrane, either spontaneously or in response to the chemokine stromal-derived factor-1alpha, was determined. Cells expressing green fluorescent protein alone were not distinguishable from untransfected or mock transfected Ba/F3 cells. However, Ba/F3 cells overexpressing full-length Crkl were found to have an increase in spontaneous migration of 2.8 +/- 0.6-fold in seven independent assays. The enhancement of migration required both the SH2 domain and the N-terminal SH3 domain. Migration in response to stromal-derived factor-1alpha was not significantly enhanced by overexpression of Crkl. Overexpression of Crkii also augmented spontaneous migration but to a lesser degree than did Crkl. Because the SH2 domain was required for enhanced migration, we looked for changes in phosphotyrosine containing proteins coprecipitating with Crkl, but not Crkl DeltaSH2, after integrin cross-linking. Full-length Crkl, but not CrklDeltaSH2, coprecipitated with a single major tyrosine phosphoprotein with an M(r) of approximately 120 kDa, identified as Cbl. The major Crkl SH3-binding protein in these cells was found to be the guanine nucleotide exchange factor, C3G. Interestingly, overexpression of C3G also enhanced migration, suggesting that a Cbl-Crkl-C3G complex may be involved in migration signaling in Ba/F3 cells. These data suggest that Crkl is involved in signaling pathways that regulate migration, possibly through a complex with Cbl and C3G.

Animals↗
PubMed2005

Survey of the migration of melamine and formaldehyde from melamine food contact articles available on the UK market.

The migration of melamine and formaldehyde, monomers used in the production of melamine-ware food contact articles, has been determined from 50 retail articles purchased in the UK. The food simulant 3% aqueous acetic acid was used as this is the most aggressive simulant towards melamine plastics. The test conditions used were repeated exposure to the simulant for 2 hours at 70 degrees C, since the articles were all intended for general use including contact with hot foods and beverages. Melamine migrated from 43 of the 50 samples tested and formaldehyde migrated from all 50 samples. Directive 2002/72/EC specifies migration limits for both of these monomers in foods and food simulants. Melamine is restricted by a specific migration limit (SML) of 30 mg/kg (equivalent to 5 mg/dm(2)) and formaldehyde, along with hexamethylenetetramine expressed as formaldehyde, is restricted by a total (T) SML(T) of 15 mg/kg (equivalent to 2.5 mg/dm(2)). In all cases the migration of melamine was much lower than the SML for this monomer. The migration of formaldehyde exceeded the SML(T) for 5 of the 50 samples tested. The failure to comply with the SML(T) was accompanied by a number of visible surface effects including discolouration and/or pitting of the simulant contact surface and cracking of the articles. Similar surface effects were observed when one of the samples was exposed to fruit juice which confirmed the suitability of the exposure conditions and 3% acetic acid as a simulant for the articles tested. The ratio of specific migration to overall migration was consistent with, but did not prove, the hypothesis that high formaldehyde migration could be due to the use of excessive hexamethylenetetramine in the polymer formulation. All illegal products were voluntarily removed from the market by the product suppliers.

Acetic Acid↗
PubMed2005

Migration of bisphenol A (BPA) from can coatings into a fatty-food simulant and tuna fish.

The effect of heat processing, storage time and temperature on the migration of bisphenol A (BPA) from organosol and epoxy can coatings to a fatty-food simulant and tuna was determined. Analyses of BPA were performed by RP-HPLC with fluorescence detection. Four migration experiments, performed between 2000 and 2003, using cans with organosol, epoxy and a combination of both types of coatings were performed under different processing conditions and storage times. Migration levels as high as 646.5 microg kg(-1) BPA from an organosol coating of tuna fish cans were found using a fatty-food simulant following the heat processing of the simulant-filled cans. Levels ranging from 11.3 to 138.4 microg kg(-1) BPA from tuna cans coated with an epoxy resin migrated to the fatty-food simulant during 1 year at 25 degrees C. Levels of BPA migration into a fatty-food simulant from thermally processed and stored tuna cans coated with a combination of organosol and epoxy resins and from vegetable cans coated with an epoxy resin were below the limit of quantitation of 10.0 microg kg(-1). Migration of BPA to tuna ranged from <7.1 to 105.4 microg kg(-1) during long-term storage at 25 degrees C. BPA levels in tuna cans purchased from three local supermarkets ranged from <7.1 to 102.7 microg kg(-1). The highest migration levels were found following heat processing at temperatures as high as 121 degrees C and at times as long as 90 min. Coatings from different can batches can give different levels of BPA migration. The migration levels of BPA found in this work are below the present European Union migration limit, except the 646.5 microg kg(-1) found after the commercial heating process was applied to the simulant-filled cans coated with the organosol resin.

Animals↗
PubMed2002

Practical experience in the use of mathematical models to predict migration of additives from food-contact polymers.

To reduce the amount of compliance-specific migration testing for food-contact polymers, the use of migration modelling has been evaluated. The paper describes experimental work carried out on a range of plastics and compares measured migrations against predictions obtained using mathematical models. A large number of experimental migration data have been obtained and used to evaluate a Fickian-based migration model in the prediction of specific migration of additives into olive oil. All tests were conducted using olive oil, representing the most severe case for fatty foods with test conditions including 2h at 121 degrees C, 6h at 70 degrees C, 2h at 70 degrees C, 2h at 60 degrees C and 10 days at 40 degrees C, representing short-term exposures at high temperatures and room temperature storage. Predicted migrations were calculated by inputting the measured initial concentration of additive in the polymers (Cp,0) into the equations together with known variables such as additive molecular weight, temperature and exposure time. The results indicate the Piringer migration model, using the 'exact' calculations of the Migratest Lite program, predicted migrations into olive oil that were close to or in excess of the experimental results and gave an overestimation for > 95% of the migrations generated here.

Food Contamination↗
PubMed1989

Laminin induces the stable expression of surface galactosyltransferase on lamellipodia of migrating cells.

We have previously shown that cell surface galactosyltransferase (GalTase) mediates cell spreading and migration on basal lamina matrices by binding N-linked oligosaccharide substrates within laminin. In this study we have examined the distribution and expression of cell surface GalTase during mesenchymal cell migration on various extracellular matrices. Antisera raised against affinity-purified beta 1,4 GalTase, as well as anti-GalTase Fab fragments, inhibited cell migration on laminin-containing matrices, whereas under identical conditions, anti-GalTase IgG had no effect on the rate of cell migration on fibronectin substrates. Cells migrating on laminin had three times the level of surface GalTase, assayed by 125I-antibody binding and by direct enzyme assay, than similar cells migrating on fibronectin. On the other hand, total cellular GalTase, assayed either enzymatically or by Northern blot analysis, was similar when cells were grown on laminin or fibronectin. The laminin-dependent increase in surface GalTase was due to its expression onto the leading and trailing edges of migrating cells in association with actin-containing microfilaments assayed by double-label indirect immunofluorescence. On stationary cells, surface GalTase levels were low, but as cells began to migrate on laminin GalTase became polarized to the growing lamellipodia. GalTase was not detectable on lamellipodia or filopodia when cells migrated on fibronectin substrates. These results show that laminin-containing matrices induce the stable expression of GalTase onto cell lamellipodia and filopodia where it mediates subsequent cell spreading and migration. Since fibronectin was unable to induce GalTase expression onto lamellipodia, these studies also suggest that the extracellular matrix can selectively influence which intracellular components are maintained on the cell surface.

Actins↗
PubMed1997

The activity of collagenase-1 is required for keratinocyte migration on a type I collagen matrix.

We have shown in a variety of human wounds that collagenase-1 (MMP-1), a matrix metalloproteinase that cleaves fibrillar type I collagen, is invariably expressed by basal keratinocytes migrating across the dermal matrix. Furthermore, we have demonstrated that MMP-1 expression is induced in primary keratinocytes by contact with native type I collagen and not by basement membrane proteins or by other components of the dermal or provisional (wound) matrix. Based on these observations, we hypothesized that the catalytic activity of MMP-1 is necessary for keratinocyte migration on type I collagen. To test this idea, we assessed keratinocyte motility on type I collagen using colony dispersion and colloidal gold migration assays. In both assays, primary human keratinocytes migrated efficiently on collagen. The specificity of MMP-1 in promoting cell movement was demonstrated in four distinct experiments. One, keratinocyte migration was completely blocked by peptide hydroxymates, which are potent inhibitors of the catalytic activity of MMPs. Two, HaCaTs, a line of human keratinocytes that do not express MMP-1 in response to collagen, did not migrate on a type I collagen matrix but moved efficiently on denatured type I collagen (gelatin). EGF, which induces MMP-I production by HaCaT cells, resulted in the ability of these cells to migrate across a type I collagen matrix. Three, keratinocytes did not migrate on mutant type I collagen lacking the collagenase cleavage site, even though this substrate induced MMP-1 expression. Four, cell migration on collagen was completely blocked by recombinant tissue inhibitor of metalloproteinase-1 (TIMP-1) and by affinity-purified anti-MMP-1 antiserum. In addition, the collagen-mediated induction of collagenase-1 and migration of primary keratinocytes on collagen was blocked by antibodies against the alpha2 integrin subunit but not by antibodies against the alpha1 or alpha3 subunits. We propose that interaction of the alpha2beta1 integrin with dermal collagen mediates induction of collagenase-1 in keratinocytes at the onset of healing and that the activity of collagenase-1 is needed to initiate cell movement. Furthermore, we propose that cleavage of dermal collagen provides keratinocytes with a mechanism to maintain their directionality during reepithelialization.

Animals↗