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PubMed2003

[Influence of urban migration on physical activity, nutritional status and growth of Senegalese adolescents of rural origin].

In Africa, rural populations especially adolescent girls resort to urban migrations for labour in order to diversify and improve their livelihood. Their work and their living conditions may influence their health and development patterns. The aim of this study was to evaluate the influence of these migrations on physical activity, nutritional and growth status of rural Senegalese adolescent girls. In 1998, within the framework of a longitudinal study of growth during puberty (n = 406), a sub-sample (n = 80, 14.4 +/- 0.5 years) was drawn in order to estimate physical activity, during three days, quantitatively by accelerometry and qualitatively by questionnaire. One part of this sample temporarily migrated to Dakar in order to work as maids (migrants, n = 40). The other part remained in the rural community of Niakhar in order to help their families in daily domestic and agricultural tasks and/or to attend school (non-migrants, n = 40). In 1999, sexual maturation of 331 adolescent girls (15.5 +/- 0.5 years) belonging to this group was based on stages of breast development and occurrence of menarche. Their growth and nutritional status were assessed with anthropometry (height, weight, mid arm circumference, six skinfolds). Adolescents were asked about their urban migratory histories and were divided into four categories according to the duration of urban migration: no migration (NM), short (S), medium (M) and long duration (L). These adolescent girls had a very high physical activity which is far higher than that of American girls. Migrants were more active than non-migrants (p < 0.0001). In 1999, as a whole, these 331 adolescent girls were smaller, thinner and less mature than adolescent girls from industrialized countries. Midarm circumference, body mass index (BMI) and fat mass index (FMI) were significantly higher with the duration of migration (p < 0.01), after adjusting for differences in sexual maturation. Growth retardation seemed more important for the adolescent girls who never migrated and for those who have the longest duration of migration (p = 0.05). At the beginning of puberty, there were no differences in height for age indice and BMI. Urban migrations resulted in an advanced puberty and an improvement of nutritional status (higher BMI, FMI and midarm circumference) but without catch-up in growth. These findings could be explained by precarious living conditions in rural area and by higher workload in urban area.

Adolescent↗
PubMed1992

Migration pathways and immunologic memory among T lymphocytes.

The lymphatic and circulatory systems are essential channels for the dissemination of memory cells throughout the body. However, the migration of naive and memory T cells through these channels is not random. Naive-type T cells preferentially migrate from blood to lymph nodes whereas memory T cells preferentially migrate to tissues, particularly those with a high exposure to antigen. The large-scaled migration of naive T cells through lymph nodes increases the likelihood of these T cells encountering a primary antigen, and brings them in contact with other players, particularly antigen presenting cells. On the other hand, the migration of memory T cells to tissues such as skin or gut mucosa serves to provide an immediate protection in an environment where antigen is likely to be re-encountered. The migration of memory T cells is further rationalized, in that phenotypically distinct subsets of memory T cells migrate to specific tissues. The migration of lymphocytes through the body is controlled by adhesion molecules on the surface of lymphocytes, which interact with receptors on the surface of endothelium, and it is the differential expression of these molecules which in part controls the different migration streams of T cells through the body.

Animals↗
PubMed2005

Gangliosides enhance migration of mouse B16-melanoma cells through artificial basement membrane alone or in presence of laminin or fibronectin.

The migration of B16LuF1 cells, B16-melanoma cells of lower metastatic potential to lung was enhanced through artificial basement membrane in presence of gangliosides of B16LuF1 cells as well as gangliosides of B16-melanoma cells of higher metastatic potential to lung, namely, B16LuF5 and B16LuF10 cells. The same concentration (50 microM) of gangliosides of B16LuF1, B16LuF5 and B16LuF10 cells gradually increased the migration of B16LuF1 cells through basement membrane. Moreover, B16LuF10 cell gangliosides modified the migratory effect of laminin and fibronectin on B16LuF1 cells. Laminin alone increased migration of B16LuF1 cells whereas fibronectin alone decreased migration of the same cells. When B16LuF10 cell gangliosides were used in combination with fibronectin, gangliosides removed the migration inhibitory effect of fibronectin resulting in net enhancing effect. Gangliosides in association with laminin also increased the enhancing effect of laminin on migration of B16LuF1 cells. Thus, gangliosides showed additive enhancing effect when used in combination with laminin. However, effect of individual gangliosides were different. Out of six gangliosides isolated from B16LuF10 cells only two gangliosides corresponding to standard gangliosides GM2 and GM3 enhanced migration of B16LuF1 cells. The migration of B16LuF1 cells in presence of each of the remaining four gangliosides corresponding to GT1b, GD1b, GD1a and GM1 was not altered and was comparable to that of untreated control. Thus, gangliosides of B16 melanoma cells alone or in combination with laminin or fibronectin enhanced migration of B16 melanoma cells through artificial basement membrane, suggesting possible role of tumor gangliosides during invasion of metastatic tumor cells through basement membrane of the surrounding tissues in vivo.

Animals↗
PubMedDate not supplied

[Downstream migration and feeding of young coho salmon Oncorhynchus kisutch in the northern part of the range in Kamchatka].

Downstream migration of young coho salmon in the northern part of the range is observed at different ontogenetic stages. Three migration periods were identified: passive migration of yearlings within the spawning river; migration of parr older than 1 year from the spawning tributary to the main river; and migration of smoltifying fish from the river to the sea. The smoltification and seaward migration of the bulk of young salmons from the Kalkaveem River takes place at the age of 2 years. Mass downstream migration of young coho salmons starts in early June at 9 degrees C. No clear diel pattern was observed in the migration of young coho salmon. The lowest migration activity was observed from sunrise to noon (3:00-12:00) when the feeding activity of young salmons increases.

Aging↗
PubMed1977

Factors which influence blood platelet migration.

Migration of human blood platelets in vitro was investigated by a modification of the capillary-tube migration chamber technique used to study the migration inhibition factor of macrophages. Platelets were packed in capillary tubes and incubated in autologous platelet-free plasma (PFP). The extent of migration was quantified by planimetry (measurement of the area of platelet migration visible by stereomicroscopy). Among the various anticoagulants employed, sodium citrate was most suitable for studying platelet migration. Optimal migration occured at 22 degrees to 37 degrees C and pH 7.2 to 7.4. Migration was inhibited by metabolic inhibitors such as iodoacetic acid, sodium fluoride, and 2,4-dinitrophenol, and inhibition was proportional to the dose of the agent added to the incubation medium. Mobility was also inhibited by cytochalasin B, which disrupts cellular microfilaments, at 1 microgram/ml PFP, but not by colchicine, a microtubule inhibitor, even at 40 microgram/ml of PFP. Light and electron microscopy showed that this inhibition was not ascribable to platelet clumping. These observations suggest that platelet mobility is an active process. The possible significance of platelet migration in hemostasis is discussed.

Anticoagulants↗
PubMed1990

Degree of platelet activating factor-induced neutrophil migration is dependent upon the molecular species.

Multiple molecular species of platelet activating factor (PAF) are produced as a result of inflammatory processes. PAF-induced neutrophil migration across endothelium is intrinsic to inflammatory responses. We therefore compared the ability of three naturally occurring PAF species (C16:0, C18:0, and C18:1), which only varied at carbon 1, to induce 51Cr-labeled human neutrophil migration across a naked 3-microns pore filter and human umbilical vein endothelial (HUVE) monolayers cultured on these filters. Time-course experiments indicated that all species of PAF tested induced significant neutrophil migration between 15 and 45 min. PAF-induced neutrophil migration through both filters alone and HUVE monolayers occurred at lower doses with C16:0 PAF. The rank order of chemotactic potency for the PAF species was C16:0 greater than C18:0 greater than C18:1 with both filters and endothelium coated filters as barriers. Intrinsic differences in the potency of these PAF molecular species to induce neutrophil chemotaxis were greater when HUVE cells were the barriers vs when filters alone were the barriers. Regardless of the molecular species used, at optimal PAF doses the degree of neutrophil migration through HUVE cells was often greater than that through filters alone. The specific PAF antagonist WEB 2086 inhibited neutrophil migration induced by all three PAF species equally. WEB 2086 pretreatment of the neutrophil or WEB 2086 coincubation with PAF, but not WEB 2086 pretreatment of the HUVE cell monolayers, significantly inhibited (65 to 80%) neutrophil migration. We conclude that the degree of PAF-induced neutrophil migration is dependent upon the molecular species of PAF. Moreover, the barrier through which the neutrophil must migrate appears to be important in influencing the overall chemotactic response to the various PAF species.

Azepines↗
PubMed1989

Vascular endothelial cell migration in vitro roles of cyclic nucleotides, calcium ion and cytoskeletal system.

According to the response to injury hypothesis, endothelial migration and repair may play an important role in the initiation and progression of atherosclerosis. In this study, we examined the regulatory mechanisms of endothelial cell migration in vitro, using cultured endothelial cells from fetal bovine aortas. Dibutyryl cyclic AMP, 8-bromo cyclic GMP, and theophylline (each at concentrations of 10(-4) to 10(-3) M) inhibited the migration of endothelial cells. Migration was not significantly affected by the Ca2+ channel blockers diltiazem (10(-6) to 10(-4) M) and nicardipine (10(-6) to 10(-5) M) or by La3+ (10(-4) to 10(-3) M), an inorganic Ca2+-antagonist, TMB-8 (10(-6) to 5 x 10(-5) M), an intracellular Ca2+ blocker, or the calmodulin inhibitors W-7 (10(-6) to 5 x 10(-5) M) and trifluoperazine (10(-7) to 10(-5) M). At the extracellular Ca2+ concentrations of less than 0.2 mEq/l, the migration was inhibited significantly. In addition, migration was markedly suppressed by colchicine (10(-8) to 10(-5) M), an inhibitor of tubulin polymerization, and by cytochalasin B (10(-7) to 10(-5) M), an inhibitor of actin polymerization. These results suggest that cyclic nucleotides, such as cyclic AMP and GMP, may regulate the migration of vascular endothelial cells. Although a low concentration of extracellular Ca2+ is essential to their migration, participation of the intracellular Ca2+-calmodulin system was not evident in this study. It appears that the cytoskeletal system, including microtubules and microfilaments, is involved in the mechanisms of migration.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

The effects of retinoic acid and butyric acid on in vitro migration by murine B16a cells: a quantitative scanning electron microscopic study.

Retinoic acid (RA) and butyric acid (BA) were investigated for their effect on in vitro migration of highly metastatic murine B16a melanoma cells. These potential antitumor agents are known to alter the cytoskeleton. Our initial studies determined the 72 h cytostatic/cytotoxic concentrations of RA (1 X 10(-6) M 1 greater than 1 X 10(-5) M) and BA (1.5 mM)/ greater than 2.0 mM). Cytostasis by RA and BA was confirmed by autoradiography and radioisotope incorporation. For migration assays, cells were plated on 3 and 5 microns diameter pore polycarbonate membranes. Complete media was added containing RA or BA at time of plating. For BA pretreatment studies, BA was added to cells for 72 h prior to plating cells in fresh BA on the membranes. Top and bottom surface of the membranes were examined after 72 h of incubation by scanning electron microscopy. Although RA and BA induced cells on top of the membrane to change morphology as shown by phase, transmission and scanning electron microscopy, only BA enhanced the deformability of cells to allow for passage through the 3 micron diameter pores. Butyric acid enhanced migration through 3 micron diameter pore membrane by 511%. For 5 micron diameter pore membranes, 55.2% of the plated number of untreated early passage cells migrated to the bottom surface as compared to 57.3% for BA-treated cells and 14.9% for RA-treated cells. However, if cellular proliferation over the 72 h period was factored in, BA increased migration by 456% over the controls and pretreatment of cells with BA for 72 h prior to plating increased migration by 893%. Without considering proliferation, RA inhibited migration by 75% over controls. The decrease in migration observed in RA-treated cells was due to an inhibitory effect on cellular migration and a decrease in proliferation.

Animals↗
PubMed1985

Cellular migration and morphology in corneal endothelial wound repair.

After a mechanical denudation of rabbit corneal endothelial cells, the healing process was followed with wide-field specular microscopy. Individual cell migration and morphologic changes were analyzed by computer-assisted morphometry. The cells surrounding the wound migrated to cover the defect without producing intercellular gaps. The greatest cellular migration and morphologic alterations occurred close to the wound edge. As the cells migrated toward the wound, they elongated and increased their surface area in the direction of the migration. As the healing proceeded, the cells lost their original hexagonal pattern, which returned after coverage was complete. The wound was covered completely by large, irregularly shaped cells showing mitotic figures between 24 and 48 hr. During this period, cellular migration decreased and normal cellular morphology began to recover. When mitosis decreased, the normal cellular pattern rearranged towards a more hexagonal shape. During the healing process, the degree and direction of cellular migration varied from cell to cell. Additionally, changes in cell-to-cell contact (positional changes of neighboring cells) occurred in one-third of migrating cells. Such cellular migration can account for monolayered cells sliding without producing gaps between individual cells.

Animals↗
PubMed1982

Effects of motilin, somatostatin, and pancreatic polypeptide on the migrating myoelectric complex in pig and dog.

Spiking activity of the gastrointestinal tract was recorded in 4 fasted pigs and 4 fasted dogs during the intravenous infusion at two rates, 5 (rate A) and 20 (rate B) ng . kg-1 . min-1 of 13-Nle-motilin, somatostatin, and bovine pancreatic polypeptide. Infusions continued for 2 h in pigs and for 5 h in dogs. 13-Nle-Motilin was unable to induce a migrating myoelectric complex or to modify its frequency in the pig at either rate of infusion. In contrast, the infusion of 13-Nle-motilin at rate B in the dog induced a migrating myoelectric complex but delayed the occurrence of the following migrating myoelectric complex. However, the mean duration (74 +/- 22 min) of the migrating myoelectric complex interval in the 5 h of infusion did not significantly change compared with the control period (92 +/- 8 min). At rate B, somatostatin inhibited the gastroduodenal spiking activity in the pig and disrupted the migrating myoelectric complex pattern, whereas this hormone at both rates of infusion increased the frequency of the migrating myoelectric complex by 69.3% and 17.2%, respectively, in the dog. The infusion of bovine pancreatic polypeptide increased the frequency of the migrating myoelectric complex significantly by 36.4% and 82% at rates A and B in the pig and by 148% at rate A in the dog. Bovine pancreatic polypeptide also inhibited spiking activity in the duodenum but not in the jejunum at rate B in the dog. These results suggest that pancreatic polypeptide, but not somatostatin, may have a regulatory function on the rhythmicity of the migrating myoelectric complex in the dog and pig and that motilin does not control the occurrence of duodenal migrating myoelectric complex in the pig.

Action Potentials↗
PubMed1983

Migration of human helper/inducer T cells in response to supernatants from Con A-stimulated suppressor/cytotoxic T cells.

Previous studies have shown that supernatants from Con A-stimulated human mononuclear cells are chemotactic for T cells, and that the source of the activity is the Leu-2 (suppressor/cytotoxic) T cell. The specificity of this chemoattractant activity for Leu-2 and/or Leu-3 (helper/inducer) T cells was analyzed with isolated human T cell subsets in an in vitro chemotaxis assay system. These studies demonstrate that both human Leu-2 and Leu-3 cells migrate in response to the lymphocyte locomotor stimulus casein, whereas only Leu-3 cells migrate in response to supernatants from Con A-stimulated mononuclear cells. This migration of Leu-3 cells to the Con A supernatant was reflected in both the distance migrated and the number of migrating cells. When Leu-2 cell locomotion in response to Con A supernatants was analyzed, no significant differences from control were observed in either the distance migrated or the number of migrating cells. Supernatants from Con A-stimulated Leu-2 cells similarly attracted Leu-3 cells but not Leu-2 cells in a concentration-dependent manner. Supernatants from Con A-stimulated Leu-3 cells did not stimulate either Leu-2 or Leu-3 cell migration. These studies demonstrate that Leu-3 T cells migrate in response to supernatants from Con A-stimulated Leu-2 T cells. This specific response may promote cell-to-cell interaction by providing a means for Leu-2 T cells to recruit Leu-3 T cells.

Chemotactic Factors↗
PubMed1980

Effect of anticancer agents on directional migration of malignant C3H mouse fibroblastic cells in vitro.

Invasion of malignant cells was considered as a target for therapy. The effect of various anticancer agents, which were known to permit or to prevent invasion in vitro, on the growth and on the directional migration of virally transformed malignant C3H mouse fibroblastic cells (MO4) was examined. The increase of the diameter of spheroidal aggregates of MO4 cells in individual shaker culture was used as an index of growth. The mean diameter of the circular area covered by cells migrating from an aggregate explanted on glass, the number of cells in the periphery of this area, the height of the central part of the aggregate, the microcinephotographic aspect of migrating cells, and the immunocytochemistry of the cytoplasmic microtubular complex were considered as indices of directional migration. Ionizing radiation (5,000 and 20,000 R), and 5-fluorouracil (0.1, 0.5, and 1 microgram/ml), known to permit invasion, inhibited growth but allowed directional migration. Nocodazole (0.1 and 1 microgram/ml), known to prevent invasion, interfered with both growth and directional migration. These observations showed that various agents which affected the growth of aggregates of MO4 cells had different effects on the directional migration of these cells; they suggested that proliferation and migration were unrelated cellular activities. The assay for directional migration of cells from a spheroidal aggregate explanted on glass is proposed for the screening of potential antiinvasive agents.

Animals↗
PubMed1993

Endotoxin activation of endothelium for polymorphonuclear leucocyte transendothelial migration and modulation by interferon-gamma.

Endotoxin [lipopolysaccharide (LPS)] is a potent inflammatory stimulus and can activate human umbilical vein endothelium (HUVE) for leucocyte adhesiveness and transendothelial migration. Here we investigated the role of HUVE-secreted cytokines in this process. When HUVE monolayers were grown on filters and preincubated for 3 hr with LPS, 51Cr-labelled polymorphonuclear leucocytes (PMNL) migrated across the HUVE in a dose- and time-dependent manner. Maximal PMNL transmigration with LPS (1 ng/ml) was 26 +/- 3% of added PMNL in 75 min. Neutralizing antibodies to interleukin-1 alpha (IL-1 alpha) and IL-1 beta, tumour necrosis factor-alpha (TNF-alpha), IL-8 or recombinant IL-1 receptor antagonist had no effect on the activation by LPS of the HUVE for supporting migration of PMNL. The HUVE 'activated state' declined with prolonged (22 hr) exposure to LPS, as reflected by a decrease in PMNL transendothelial migration to 5.5 +/- 1% and in the expression of the endothelial cell adhesion molecule, E-selectin, as compared to stimulation with LPS for 3 hr. However, simultaneous exposure to interferon-gamma (IFN-gamma) (200 IU/ml) and LPS maintained maximal PMNL transendothelial migration (28 +/- 4%) for at least 24 hr, prolonged E-selectin expression by HUVE and superinduced intracellular adhesion molecule-1 (ICAM-1) expression. The PMNL transendothelial migration was blocked by > 90% by monoclonal antibody (mAb) to CD18 with either 3 hr of LPS or 22 hr LPS + IFN-gamma stimulation. Migration was partially inhibited by mAb to E-selectin (30-40%) or to ICAM-1 (35-45%) and by a combination of both reagents (50-60%) under both stimulation conditions. Thus, LPS activation of HUVE for PMNL transendothelial migration: (a) does not require secretion of IL-1, TNF-alpha or IL-8 by the endothelium, (b) IFN-gamma enhances and prolongs endothelial activation by LPS and may increase leucocyte infiltration in LPS or bacterial inflammatory reactions, and (c) CD18-dependent mechanisms are equally important for PMNL transendothelial migration under both acute (3 hr) and prolonged (22 hr LPS + IFN-gamma) activation of endothelium.

Antibodies, Monoclonal↗
PubMed1994

Mesangial cell migration precedes proliferation in Habu snake venom-induced glomerular injury.

BACKGROUND: Mesangial cells migrate in response to platelet released products in vitro (Am J Pathol 1991;138:859). Cell migration, in addition to proliferation might play a role in cell remodeling during the course of proliferative glomerular disease. EXPERIMENTAL DESIGN: In this study, we examined mesangial cell migration in vivo in a platelet-dependent model of proliferative glomerulonephritis induced by Habu snake venom. Mesangial cell migration was assessed by phenotypic identification and temporal location of mesangial cells within glomerular lesions in serial time studies from 8 to 48 hours after Habu snake venom. Autoradiography of [3H]thymidine incorporation into cells was employed to identify and temporally separate cell division and proliferation from cell motility and other related events. RESULTS: Early (8-hour) lesions consisted of microaneurysms devoid of mesangial cells. By 24 hours, glomeruli showed mesangial cells at the margins of lesions adjacent to intact glomerular tufts, followed by the presence of clusters of cells at 30 and 36 hours. By 48 hours, most lesions were filled with proliferating mesangial cells. Cells containing [3H]thymidine were rarely observed until 30 hours, at which point they were found in advanced lesions. Marginating cells did not contain [3H]thymidine, suggesting that the location of these cells was not related to cell division but rather to migration. Platelet depletion eliminated platelets from lesions and substantially retarded mesangial cell migration into glomerular lesions indicating mesangial cell migration is, in part, dependent on platelets or their secretory products. CONCLUSIONS: These studies show that mesangial cells can migrate in vivo and suggest that cell migration is an important early step in cell redistribution and remodeling during glomerular injury in this model of proliferative glomerulonephritis.

Animals↗
PubMed1993

Type IV collagen, laminin, and fibronectin promote the adhesion and migration of rabbit lens epithelial cells in vitro.

PURPOSE: To assess the ability of basement membrane and extracellular matrix proteins to promote rabbit lens epithelial cell adhesion and migration, which may play a role in the development of secondary cataract. METHODS: Rabbit lens epithelial cells were isolated and grown in tissue culture for use in standardized assays to study adhesion and migration of rabbit lens epithelial cells in response to type IV collagen, laminin, fibronectin, and ovalbumin. RESULTS: Under these conditions, the adhesion of rabbit lens epithelial cells to surfaces coated with varying concentrations of type IV collagen, laminin, and fibronectin was shown to be dependent on concentration. Rabbit lens epithelial cells did not adhere to ovalbumin-coated surfaces at any concentration tested. Type IV collagen promotes maximal in vitro adhesion of rabbit lens epithelial cells at lower coating concentrations in comparison to laminin and fibronectin. In cell migration experiments, fibronectin promoted maximal migration at lower concentrations in comparison with laminin and type IV collagen. This was shown both in haptotaxis experiments (the migration of cells to surfaces coated with protein) and in chemotaxis experiments (the migration of cells to attractants in solution). Lens epithelial cells did not migrate in response to ovalbumin under the conditions of this study. CONCLUSION: The results of these studies indicate that adhesion and migration of lens epithelial cells occurs in response to the lens capsule proteins type IV collagen and laminin and in response to fibronectin, a protein found in the lens during embryologic development. Because fibronectin plays a role in the embryologic development of the lens but is not normally present in the adult lens, the possible introduction of fibronectin into the eye after surgery may play a critical role in the posterior migration of lens epithelial cells and the development of posterior capsular opacification or secondary cataract.

Animals↗
PubMed1993

Multiple receptor systems promote CNS neural migration.

To identify glial receptor systems in CNS migration, cerebellar granule neuron migration was assayed on glass fibers coated with polylysine, astroglial membranes (AM fibers), or the extracellular matrix proteins collagen (COLL fibers), fibronectin (FN fibers), and laminin (LAM fibers). By video microscopy, granule cells migrated along AM fibers with the cytology, neuron-fiber apposition, and dynamics seen on living glia. The demonstration that immobilized astroglial membranes support neural migration suggests that astroglial receptor systems, in combination with glial fiber geometry, promote CNS neural migration. Moreover, granule neurons migrated rapidly on LAM fibers, moved relatively slowly on FN fibers, and not at all on COLL fibers. Antibody perturbation analyses suggested that, whereas astrotactin provides the neural receptor for migration on astroglial membranes, integrin beta 1 provides the neural receptor for migration on LAM fibers. These results suggest that multiple receptor systems support CNS neural migration.

Animals↗
PubMed1996

Directed migration of corneal epithelial sheets in physiological electric fields.

PURPOSE: To characterize the effects of small applied electric fields (EFs) (100 to 250 mV/ mm) on cultured bovine corneal epithelial cell (CEC) sheets and to determine how EFs interact with other environmental cues in directing CEC sheet migration. METHODS: Primary cultures of bovine CECs were exposed to EFs in medium with or without serum, epithelial growth factor, basic fibroblast growth factor, or transforming growth factor-beta 1. Cell sheet migration was traced using an image analyzer. RESULTS: Cell sheets migrated toward the cathode (negative pole). The directional migration was voltage dependent, and, at low field strength (up to 200 mV/mm), it required serum in the medium. Sheets showed no migration responses up to 200 mV/mm in serum-free medium, whereas those in medium with serum showed evident migration toward the cathode, at an average rate of approximately 15 microns/h (n = 15 approximately 20) at 150 mV/mm. When serum was present, the threshold was below 100 mV/mm, very close to the measured wound field strength (approximately 42 mV/mm). After supplementing serum-free medium with individual growth factors or with combinations of epithelial growth factor, basic fibroblast growth factor, and transforming growth factor-beta 1, significant restoration of cathode-directed migration occurred at 150 mV/ mm. Lamellipodia were abundant at the leading edges of migrating sheets, extending the area of sheets covered. The extension of cell membranes toward the cathode was more prominent in cell sheets than in single cells. CONCLUSIONS: The endogenous EFs generated by wounded cornea could play an important role by interacting with other environmental factors to promote changes in shape and in directed migration of CEC sheets.

Animals↗
PubMed1997

Migration of highly aggressive MV3 melanoma cells in 3-dimensional collagen lattices results in local matrix reorganization and shedding of alpha2 and beta1 integrins and CD44.

The three-step model of cell migration consisting of protrusion of a leading lamella, attachment to the substrate, and contraction of the cell body is well established for fibroblasts migrating across planar surfaces. However, it is not resolved to what extent the migration of cancer cells in a 3-dimensional tissue environment follows similar principles. Here, we present evidence that the migration of highly invasive MV3 melanoma cells in 3-dimensional collagen matrices follows the three-step concept of migration but also results in characteristic reorganization of the extracellular matrix. After incorporation in the lattice, MV3 cells spontaneously developed a slow type of migration (mean velocity, 0.19 microm/min), leading to alignment of collagen fibers at attachment sites, as detected from unfixed and fixed samples by confocal reflection contrast in combination with immunofluorescence staining. In the process of migration, the formation of focal clusters or stripes of alpha2 and beta1 integrins colocalized with binding sites to collagen fibrils at the leading as well as the trailing edge. In contrast, CD44 was nonclustered and redistributed toward the rear end of the cell. At detachment sites, dynamic fiber traction, localized fiber disruption, and the release of cell surface determinants, including alpha2beta1 integrins and CD44, resulted in circumscribed matrix reorganization. Not infrequently, these emerging tube-like paths of least resistance bordered by a dense fiber network facilitated the reorientation and contact guidance of proximate MV3 cells to migrate along the preexisting path. In conclusion, the migration of MV3 cells in 3-dimensional collagen lattices resulted in dynamic tissue reorganization and receptor shedding the consequences of which were directly visualized by combining confocal reflection imaging with immunofluorescence.

Animals↗