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At least 145 records · Page 8Linked to original sources
PubMed2002

Use of fluorescently labelled deoxyribonuclease I to spatially measure G-actin levels in migrating and non-migrating cells.

Lamellipodium protrusion is linked to actin filament disassembly in migrating fibroblasts [Cramer, 1999: Curr. Biol. 9:1095-1105]. To further study this relationship, we have identified a method to specifically and sensitively detect G-actin in distinct spatial locations in motile cells using deoxyribonuclease I (DNase I). Although DNase I can bind both G- and F-actin in vitro [Mannherz et al., 1980: Eur. J. Biochem. 95:377-385], when cells were fixed in formaldehyde and permeabilized in detergent, fluorescently-labelled DNase I specifically stained G-actin and not F-actin. 92-98% of actin molecules were stably retained in cells during fixation and permeabilization. Further, increasing or decreasing cellular G-actin concentration by treating live cells with latrunculin-A or jasplakinolide, respectively, caused a respective increase and decrease in DNase I cell-staining intensity as expected. These changes in DNase I fluorescence intensity accurately reflected increases and decreases in cellular G-actin concentration independently measured in lysates prepared from drug-treated live cells (regression coefficient = 0.98). This shows that DNase I cell-staining is very sensitive using this method. Applying this method, we found that the ratio of G-/F-actin is lower in both the lamellipodium and in a broad band immediately behind the lamellipodium in migrating compared to non-migrating fibroblasts. Thus, we predict that protrusion of the lamellipodium in migrating fibroblasts requires tight coupling to filament disassembly at least in part because G-actin is relatively limited within and behind the lamellipodium. This is the first report to directly demonstrate high sensitivity of cell-staining for any G-actin probe and this, together with the ready commercial accessibility of fluorescently-labelled DNase I, make it a simple, convenient, and sensitive tool for cell-staining of G-actin.

3T3 Cells↗
PubMedDate not supplied

Growth cone migration across extracellular matrix components depends on integrin, but migration across glioma cells does not.

To promote neurite elongation, nerve growth cones must adhere to other surfaces. A complex of integral membrane glycoproteins mediates cell binding to the extracellular glycoproteins fibronectin and laminin (Horwitz et al., J Cell Biol 101:2134-2144, 1985). The receptor complex, named integrin, binds to fibronectin by recognition of a specific peptide sequence, Arg-Gly-Asp-Ser (RGDS), in the fibronectin molecule (Pierschbacher and Ruoslahti, Proc Natl Acad Sci USA 81:5985-5988, 1984). We have used antibodies to integrin and an RGDS synthetic peptide to probe the functions of integrin in the migration of growth cones extended from sensory and spinal cord neurons of chick embryos. Analyses of time lapse videotapes of growth cone migration before and after adding RGDS indicated that 2 mM RGDS rapidly inhibits growth cone movement on substrata coated with fibronectin or a fragment of fibronectin containing the RGDS sequence. RGDS has no effect on growth cone movement on laminin or on a surface coated with material deposited from heart conditioned medium. However, a monclonal antibody to the integrin complex (10 micrograms/ml CSAT) completely blocks growth cone movement on substrata treated with fibronectin, laminin, or heart conditioned medium. Thus integrin may be involved in growth cone adhesion to several extracellular molecules, although the selective effects of RGDS indicate that the integrin complex may have heterogeneous sites for interaction with different components of the extracellular matrix. CSAT antibody has no discernible effect, however, on growth cone migration across the upper surfaces of C6 glioma cells. These data indicate that the surfaces of nerve growth cones contain multiple binding molecules that mediate different adhesive interactions during migration.

Animals↗
PubMed1994

LHRH cells migrate on peripherin fibers in embryonic olfactory explant cultures: an in vitro model for neurophilic neuronal migration.

Luteinizing hormone releasing hormone (LHRH) neurons arise from progenitor cells in the olfactory placode. During prenatal development, these cells migrate via neurophilic interactions, in track-like arrangements along axons of the olfactory complex. The mechanisms by which these cells attain an adult-like distribution are unknown. In this study, we established an in vitro, embryonic mouse olfactory explant model to examine the factors directing LHRH cell migration. Cultures were generated from E11.5 embryos and maintained for up to 3 weeks. Typically 20-50% (160-400 LHRH cells) of the total LHRH neuronal population survived and maintained gene expression in these explants. Fibronectin and laminin staining delineated substratum producing cells which concentrically spread, from Days 1-7, from the periphery of the entire explanted tissue. In contrast, LHRH cells emigrated exclusively from inside olfactory pit areas to the surface of the culture after 3 days. The relationship between groups of LHRH cells emerging from bilateral olfactory pits was not random, but highly organized; in 93% of the cultures examined, the angular relationship between these groups was 180-270 degrees. After 5 or more days in vitro, LHRH cells were found in directional tracks similar to those observed in vivo forming a continuum from the olfactory pit out onto the substratum, where many bipolar LHRH cells were discretely located. The maximum distance away from the olfactory pit that LHRH cells were detected was 0.9 mm, which is compatible with the distance traversed by LHRH cells through the nasal region in vivo. The reproducible spatiotemporal appearance of LHRH cells was unrelated to the concentric spread of the fibronectin and laminin producing cells of the explant. Taken together, these data indicate that LHRH cells migrated directionally in these explants and that the molecular cues governing the initial migration of these neurons remained intact in this system in the absence of brain tissue. Double-label immunocytochemistry indicated that at least three populations of neuronal fibers existed in the explants: N-CAM-positive, peripherin-positive, and N-CAM/peripherin-positive. Although all three fibers groups showed highly organized spatiotemporal distribution patterns, only peripherin-positive fibers correlated with the location of LHRH cells. LHRH cells were always preceded by, and in close association with, peripherin-positive fibers. We hypothesize that signals arising from the peripherin-positive axons provide the appropriate guidance cues to LHRH cells as they emigrate from the olfactory pit.

Animals↗
PubMed1990

A fibronectin-related synthetic peptide, Pro-Ala-Ser-Ser, inhibits fibronectin binding to the cell surface, fibronectin-promoted cell migration in vitro, and cell migration in vivo.

The biological activity of the amino acid sequence consisting of the immediate carboxyl terminus side of the Arg-Gly-Asp-Ser (RGDS) amino acid sequence in the cell-binding domain of intact fibronectin (FN) molecules was examined using synthetic peptides [RGDS, Gly-Arg-Gly-Asp-Ser-Pro (GRGDSP), Arg-Gly-Asp-Ser-Pro-Ala-Ser-Ser-Lys-Pro (RGDSPASSKP), Pro-Ala (PA), Pro-Ala-Ser (PAS), Pro-Ala-Ser-Ser (PASS), and Pro-Ala-Ser-Ser-Lys (PASSK)]. These peptides were applied to the primary mesenchyme cells (PMCs) of the sea urchin, Clypeaster japonicus. In vitro immunohistochemistry indicated that the binding of exogenous FN to the PMC surface was inhibited by the peptides RGDSPASSKP and PASS, but not by RGDS, GRGDSP, PA, or PAS. PASS and RGDS introduced into the blastocoel also inhibited PMC migration in vivo. FN-promoted PMC migration in vitro was also inhibited by PASS and RGDS. The present results indicate that the PASS peptide inhibits FN binding to the PMC surface and promotes PMC migration, suggesting that the FN molecule uses the PASS amino acid sequence to bind to the PMC surface and to promote PMC migration in the blastocoel.

Amino Acid Sequence↗
PubMed1992

The EGF-inducible protein EIP-1 of migrating normal and malignant rat liver epithelial cells is identical to plasminogen activator inhibitor 1 and is a component of the ECM migration tracks.

Induction of rat liver epithelial cell migration by epidermal growth factor (EGF) changes the expression pattern of secreted proteins. The expression of the early induced glycoprotein EGF-inducible protein No. 1 (EIP-1) correlates with the migratory behavior of both normal and Ha-ras-transformed, tumorigenic cells and is deposited into the ECM migration tracks. The sequence of two clones from a cDNA library of EGF-induced cells and the amino terminal sequence of the purified protein revealed that EIP-1 is identical to rat plasminogen activator inhibitor 1 (PAI-1). Based on the migration-linked expression pattern of EIP-1/PAI-1 it is proposed that the inhibitor is required for the migration of these cells, but not sufficient to stimulate it.

Animals↗
PubMed1992

Activation of a C. elegans Antennapedia homologue in migrating cells controls their direction of migration.

Anterior-posterior patterning in insects, vertebrates and nematodes involves members of conserved Antennapedia-class homeobox gene clusters (HOM-C) that are thought to give specific body regions their identities. The effects of these genes on region-specific body structures have been described extensively, particularly in Drosophila, but little is known about how HOM-C genes affect the behaviours of cells that migrate into their domains of function. In Caenorhabditis elegans, the Antennapedia-like HOM-C gene mab-5 not only specifies postembryonic fates of cells in a posterior body region, but also influences the migration of mesodermal and neural cells that move through this region. Here we show that as one neuroblast migrates into this posterior region, it switches on mab-5 gene expression; mab-5 then acts as a developmental switch to control the migratory behaviour of the neuroblast descendants. HOM-C genes can therefore not only direct region-specific patterns of cell division and differentiation, but can also act within migrating cells to programme region-specific migratory behaviour.

Animals↗
PubMed2005

Contact stimulation of prostate cancer cell migration: the role of gap junctional coupling and migration stimulated by heterotypic cell-to-cell contacts in determination of the metastatic phenotype of Dunning rat prostate cancer cells.

BACKGROUND INFORMATION: Motile activity of tumour cells is regarded as a critical factor determining their metastatic potential. We have shown previously that contrary to the majority of normal cells, homotypic contacts between some tumour cells, among them low metastatic (AT-2) and highly metastatic (MAT-LyLu) rat prostate cancer cells, increase the speed of their movements. The aim of the present study was to determine the effect of heterotypic cell-to-cell contacts on the migration of rat prostate cancer cells differing in metastatic potential, and to correlate it with the intensity of homo- and heterologous gap junctional coupling. RESULTS: MAT-LyLu and AT-2 cells moving on the surface of fibroblasts displayed significantly greater cell displacement than those moving on plastic substrata. This effect correlated with the polarization (contact guidance) and increased speed of cell movements. However, in contrast with the migration on plastic substrata, where MAT-LyLu cells displayed considerably higher motility than AT-2 cells, no differences between both cell lines were observed on the surface of fibroblasts. On the other hand, in contrast with AT-2, Mat-LyLu cells displayed extensive homologous coupling mediated by connexin43 and were able to couple with normal fibroblasts. CONCLUSION: Heterotypic contacts between migrating prostatic cancer cells and normal fibroblasts can strongly stimulate their migration during invasion; however, this effect does not correlate with the gap junctional coupling between cancer cells and normal fibroblasts.

Animals↗
PubMed1997

Keratocyte migration and peptide growth factors: the effect of PDGF, bFGF, EGF, IGF-I, aFGF and TGF-beta on human keratocyte migration in a collagen gel.

PURPOSE: Peptide growth factors are known accelerators of corneal wound healing, probably mediated through increased proliferation of the cells; however, information about their effect on keratocyte motility is lacking. The influence of peptide growth factors on keratocyte migratory activity was investigated, using the following growth factors: platelet derived growth factor (PDGF-BB), epidermal growth factor (EGF), acidic fibroblast growth factor (aFGF), basic fibroblast growth factor (bFGF), insulin-like growth factor-I (IGF-I) and transforming growth factor-beta-1 (TGF-beta 1). METHODS: Keratocytes were seeded on gels of type 1 collagen, growth factor added, and the cells left to migrate for 72 hours. Subsequently, the number of keratocytes at the different levels in the collagen gel was evaluated by optically sectioning the gel at 20 microns, intervals, with an inverted phase contrast microscope. RESULTS: PDGF, EGF and bFGF at 10 ng/ml, all increased the number of keratocytes at the different levels of the gel as compared to a non-stimulated control (p < 0.05 or p < 0.01, students t-test). TGF-beta proved to be a strong inhibitor of keratocyte migration, decreasing the number of keratocytes observed at every level in the gel (p < 0.05 and p < 0.01, students t-test), whereas no effect of IGF-I and aFGF was found. During the 72 hours of migration, no contraction of the collagen gels was observed. Autoradiography of histological sections of the gels showed that during the 72-hour period only TGF-beta and 10% fetal bovine serum induced an increase in keratocyte proliferation. CONCLUSION: PDGF, EGF and bFGF increase keratocyte migration, independent of proliferation in a collagen gel invasion assay and might promote corneal wound healing, not only by increasing cell proliferation, but also through increased motility.

Autoradiography↗
PubMed2004

Migration from can coatings: part 3. Synthesis, identification and quantification of migrating epoxy-based substances below 1000 Da.

Bisphenol A-derived glycidyl ethers as well as its reaction products with other lacquer components can migrate into the packed food from epoxy-based can coatings. A sensitive and selective method is presented using high-performance liquid chromatography coupled with ultraviolet light, fluorescence and electrospray ionization-mass selective detection for the identification and quantification of all migrants with a bisphenol A backbone and a molecular weight below 1000 Da, an estimated boundary for the absorption in the gastrointestinal tract. The identification of migrants was confirmed by microreactions of technical bisphenol A diglycidyl ether with solvents and phenols, which provided the fragmentation pattern of the mass selective detection and relative retentions of 42 different bisphenol A-related substances. It was shown by calibration of different isolated and synthesized bisphenol A derivatives that the fluorescence response relies on the amount of bisphenol A moiety in the respective molecule. Therefore, all migrating bisphenol A-related substances below 1000 Da were determined as bisphenol A diglycidyl ether equivalents using a calibration (fluorescence detection) of the commercially available bisphenol A diglycidyl ether monomer. The limit of quantification was set at 5 microg bisphenol A diglycidyl ether equivalents kg(-1) (or 0.8 microg dm(-2)). This method was validated for epoxy coatings (0.1 microg dm(-2) limit of detection and 24 microg bisphenol A-related substances below 1000 Da dm(-2) standard deviation, corresponding to 4.4% relative standard deviation). The quantification could be extended by combining the fluorescence response and structural information gained from the mass spectra, which provides more accurate results for each migrant. The calculation is based on the calibration of the bisphenol A chromophore content of the molecule. According to this method, the amount of migrating bisphenol A-related substances below 1000 Da in the acetonitrile extract (assuming a worst case) varied from about 0.4 to 0.7 mg dm(-2) in the examined coatings. The determined amounts comply with about 50% of the total migrate below 1000 Da.

Benzhydryl Compounds↗
PubMed2005

Neuronal migration defects in cerebellum of the Largemyd mouse are associated with disruptions in Bergmann glia organization and delayed migration of granule neurons.

The Large gene encodes a putative glycosyltransferase that is required for normal glycosylation of dystroglycan, and defects in either Large or dystroglycan cause abnormal neuronal migration. The mechanism for this effect is not fully understood. This study analyzes the Largemyd mouse cerebellum during postnatal cerebellar development. Large is shown to be expressed most strongly in the Bergmann glial cells and Purkinje cells throughout cerebellar development, which is similar to what is known for dystroglycan expression. Discontinuities of the pial surface of the developing Largemyd mouse cerebellum correlate with disruption of the normal organization of the external granule cell layer and Bergmann glial fibers. At early time points, granule neurons express differentiation markers normally, both temporally and spatially, and show no defects in neurite outgrowth in in vitro assays. However, granule neuron migration is delayed within the external granule and molecular layers, resulting in granule neurons undergoing their intrinsically programmed differentiation in inappropriate locations. Consequently, cells expressing mature granule neuron markers become stranded within these layers. The cause of the less efficient migration is likely due to both physical disruption of the glial-guide scaffolding, as well as to suboptimal neuronal-glial guide interactions during migration.

Animals↗
PubMed1983

Microtubule-organizing centers and cell migration: effect of inhibition of migration and microtubule disruption in endothelial cells.

We have previously shown that microtubule-organizing centers (MTOC's) become preferentially oriented towards the leading edge of migrating endothelial cells (EC's) at the margin of an experimentally induced wound made in a confluent EC monolayer. To learn more about the mechanism responsible for the reorientation of MTOC's and to determine whether a similar reorientation takes place when cell migration is inhibited, we incubated the wounded cultures with colcemid (C) and cytochalasin B (CB), which disrupt microtubules (MT's) and microfilaments (MF's), respectively. The results obtained showed that the MTOC reorientation can occur independent of cell migration since MTOC's reoriented preferentially toward the wound edge in the CB-treated cultures, even though forward migration of the EC was inhibited. In addition, the MTOC reorientation is inhibited by C, indicating that it requires an intact system of MT's and/or other intracellular structures whose distribution is dependent on that of MT's.

Animals↗
PubMed1994

Migration of murine epidermal Langerhans cells to regional lymph nodes: engagement of major histocompatibility complex class II antigens induces migration of Langerhans cells.

Langerhans cells are resident dendritic cells in the epidermis. Once they are loaded with epicutaneously-delivered antigens, they leave the epidermis and migrate to the regional lymph nodes where they initiate primary T cell responses as antigen-presenting cells. However, the stimulus that initiates such migration remains unknown. Because major histocompatibility complex class II (Ia) antigens on B lymphocytes or monocytic cells have been shown to function as signal transducers, we evaluated the effect of the engagement of Ia antigens on the migration of murine epidermal Langerhans cells. The intradermal injection of an anti-Ia monoclonal antibody (mAb) reduced the density of Langerhans cells in epidermis and produced a dose- and time-dependent increase in the frequency of cells reactive with NLDC145 (Langerhans cell- and dendritic cell-specific mAb) within the regional lymph nodes. Injection of a control mAb had no effect. The NLDC145+ cells that were induced to accumulate in the regional lymph nodes were Ia+, large dendritic cells, some of which were positive for both NLDC145 and F4/80, a phenotype corresponding to that of murine epidermal Langerhans cells. Thus, the engagement of Ia antigens on Langerhans cells by mAb induces the migration of Langerhans cells from the epidermis to the regional lymph nodes. Analysis of these changes in Langerhans cells in vitro may help to reveal the biochemical sequence of events involved in the activation and differentiation of Langerhans cells.

Animals↗
PubMed1990

Seasonal migration as a substitute for, or precursor to, permanent migration.

Seasonal migration to national amenity areas is a major form of cyclical migration in the United States. This article examines conditions under which seasonal movement serves as a substitute for, or precursor to, permanent migration among winter visitors to recreational vehicle (RV) parks in the Phoenix, Arizona area. Ties to the home community, ties to the seasonal residence, demographic characteristics, and commitment to a mobile lifestyle are specified as determinants of expectations of moving to Phoenix on a permanent basis. The model is tested using survey data for a sample of 1,001 winter visitors in Phoenix RV parks. Results of a discriminant analysis indicate that place ties and position in the life cycle condition expectations of permanently migrating to a seasonal residence.

Age Factors↗
PubMed2025

Policy paper of the Committee on Ethics and Task Force on Migration and Mental Health: Migration and mental health of migrants, refugees, asylum seekers - Ethical dilemmas and concerns.

BACKGROUND: International migration is a complex phenomenon of global and historical relevance. It includes voluntary, forced, and workforce migration, shaped by diverse determinants. Push factors comprise war, persecution, and political instability, while pull factors include stability, economic opportunities, education, and favorable living conditions. Forced migration is frequently associated with displacement and a disproportionate burden of mental health disorders, which are urgent yet difficult to address due to structural, cultural, and legal barriers. METHODS: Evidence demonstrates that restricted health care access exacerbates psychiatric disorders, while treatment delays contribute to poorer outcomes. Barriers include administrative limitations, linguistic and cultural differences, stigma, and resource shortages. This policy paper was developed by the Committee on Ethics and the Task Force on Migration and Mental Health of the European Psychiatric Association (EPA). Relevant literature was reviewed and combined with the professional expertise of committee members. The draft was subsequently evaluated by the Publication Committee and the EPA Board, and revised accordingly. RESULTS: Ethical principles in refugee care are insufficiently implemented in many European countries. Core principles of medical ethics - beneficence, respect for autonomy, non-maleficence, and justice - as well as the obligation to advance psychiatric standards and apply psychiatric expertise for societal benefit, are inconsistently upheld. CONCLUSIONS: The primary duty of physicians is to promote health and well-being through competent, timely, and compassionate care. The EPA therefore advocates coordinated strategies to mitigate the mental health consequences of war, displacement, and trauma, and to secure equitable access to psychiatric services for migrants and refugees.

Humans↗
PubMed1991

Type IV collagen and corneal epithelial adhesion and migration. Effects of type IV collagen fragments and synthetic peptides on rabbit corneal epithelial cell adhesion and migration in vitro.

Type IV collagen, a 500-kilodalton (alpha 1)2(alpha 2)1 heterotrimer with noncollagenous domains (NC1) is the major molecule in most basement membranes in the body. In addition to its structural role as scaffolding, type IV collagen is involved in promoting adhesion and migration of various cell types in vitro, including rabbit corneal epithelial cells. This study assessed the effect of purified proteolytic fragments of type IV collagen and selected synthetic peptides derived from the alpha 1 and alpha 2 chains that are related to the adhesion and directed migration of dissociated primary cultured rabbit epithelial cells. Two homologous peptides (HEP-1 and HEP-2) derived from alpha 1 and alpha 2 NC1 regions were found to promote epithelial cell adhesion. A peptide (HEP-3) derived from an interruption of the triple helix of type IV collagen was effective in promoting corneal epithelial cell migration in both chemotaxis and haptotaxis assays. The helical fragment of type IV collagen promoted both directed migration and ample adhesion, indicating that there may be at least another moiety in the helical region responsible for cell adhesion. The results with these peptides revealed to some extent how corneal epithelial cells react at the molecular level with type IV collagen. They could serve as the basis for therapeutic agents to modify corneal epithelial behavior in situations of perturbed wound healing.

Amino Acid Sequence↗
PubMedDate not supplied

New FDA migration cell used to study migration of styrene from polystyrene into various solvents.

A new cell was evaluated for studying the migration of components of plastic food packaging materials into various food simulating solvents. Data obtained using this cell to study the migration of styrene from polystyrene at 40 and 70 degrees C are presented. Food simulating solvents tested were: water; 3% acetic acid; 8, 20, 50, and 100% ethanol; corn oil; HB-307; heptane; hexadecane; and decanol. An iterative Basic computer program is described that fits the migration vs time data obtained to mathematical models, based on Ficks' law, yielding migrant/polymer diffusion coefficients (Dp). Dp values determined for styrene migration from polystyrene at 40 and 70 degrees C were 3 X 10(-13) and 4 X 10(-12) sq. cm/s, respectively.

Chemical Phenomena↗
PubMed1986

Radiation leukemia virus-transformed immunocompetent T cells. II. Antigen-induced macrophage migration inhibition factor and leukocyte migration inhibition factor production.

OVA-specific T cells were immortalized by infection with radiation leukemia virus (RadLV). Some clones derived from such population were shown to exhibit helper activity. We then tested clones without such function and found among them some that secreted macrophage migration inhibition factor (MIF) and leukocyte migration inhibition factor (LIF) upon exposure to the antigen in vitro. The lymphokine-producing clones, which were Thy-1+, Ly-1+ and Ly-2-, did not secrete MIF and LIF constitutively. Like other antigen-specific T cells, the immortalized clones could not be stimulated by free soluble antigen but required macrophages for presentation and for triggering the lymphokine production. The antigen-activated clones exclusively produced MIF and LIF, but not interleukin 2 or colony-stimulating factor. They neither provided helper activity nor induced delayed-type hypersensitivity. The data suggest that the T-cell clones carry the antigen receptors and that their antigen-inducible biological function is restricted to the migration inhibitory factor production.

Animals↗
PubMed1981

The short-run dynamics of inter-state migration: a space-time economic adjustment model of in-migration to fast growing states.

"Interregional migration is analyzed with respect to its short-run responsiveness to economic fluctuations and its efficiency as a spatial labour market allocation mechanism. Using a space-time analytical framework, in-migration to four fast growing States of the United States is analyzed over the period 1958-1975. It is shown via a time-series model, employing a Koyck-distributed lag methodology, that short-run in-migration is in fact responsive to economic fluctuations." (SUMMARY IN FRE, GER)

Americas↗