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PubMed2000

Interleukin-8 and leukotriene-B(4), but not formylmethionyl leucylphenylalanine, stimulate CD18-independent migration of neutrophils across human pulmonary endothelial cells in vitro.

Although neutrophil migration from the systemic circulation involves the beta2- (or CD18) integrin family, the existence of an alternative, CD18-independent route of neutrophil extravasation to tissues has been demonstrated in animal models. The molecular interactions involved in this alternative migratory route have not yet been characterized. The objective of this study was to assess the CD18-dependency of neutrophil migration across human endothelial cells from an organ known to support CD18-independent migration, the lung, with a view to establishing an in vitro model to facilitate study of CD18-independent migration. Neutrophil migration across human pulmonary artery endothelial cells (HPAECs) in response to three different chemoattractants, formylmethionyl leucylphenyl-alanine (FMLP), interleukin (IL)-8, and leukotriene (LT) B(4), was examined. Results demonstrated that a function-blocking antibody to CD18 decreased FMLP-stimulated migration by 71.7 +/- 4.4% (P < 0.001). In contrast, migration in response to LTB(4) was decreased by only 20.5 +/- 10.2% (P < 0.01), and no significant decrease was observed with migration to IL-8. Neutrophils that migrated to FMLP had 1.7-fold more surface CD11b/CD18 compared with nonmigrated neutrophils (P < 0.01), whereas this integrin complex was not significantly upregulated on neutrophils that had migrated to IL-8 or LTB(4). Further investigation of this migratory route indicated that it did not involve the beta1 integrins (CD29) or the endothelial selectins, E- or P-selectin, nor did it require the activity of either metalloproteinases or neutrophil elastase. These results indicate that neutrophil migration across HPAECs in vitro to IL-8 and LTB(4) is predominantly CD18-independent and provides a much-needed in vitro system for examination of the neutrophil-endothelial interactions involved in this alternative migratory route.

CD11 Antigens↗
PubMed1995

Nitric oxide inhibits angiotensin II-induced migration of rat aortic smooth muscle cell. Role of cyclic-nucleotides and angiotensin1 receptors.

Nitric oxide (NO) and angiotensin II (AII) can effect vascular smooth muscle cell (SMC) proliferation. However, the effects of such agents on SMC migration, an equally important phenomenon with regard to vascular pathophysiology, have received little attention. The objectives of the present study were: (a) to determine whether NO inhibits AII-induced migration of vascular SMCs; (b) to investigate the mechanism of the interaction of NO and AII on SMC migration; and (c) to evaluate the AII receptor subtype that mediates AII-induced SMC migration. Migration of rat SMCs was evaluated using a modified Boydens Chamber (transwell inserts with gelatin-coated polycarbonate membranes, 8 microns pore size). AII stimulated SMC migration in a concentration-dependent manner, and this effect was inhibited by sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP). In the presence of L-arginine, but not D-arginine, IL-1 beta, an inducer of inducible NO synthase, also inhibited AII-induced SMC migration, and this effect was prevented by the NO-synthase inhibitor, N-nitro-L-arginine methyl ester. The effects of NO donors on AII-induced SMC migration were mimicked by 8-bromo-cGMP. Also, the antimigratory effects of SNAP were partially inhibited by LY83583 (an inhibitor of soluble guanylyl cyclase) and by KT5823 (an inhibitor of cGMP-dependent protein kinase). Although 8-bromo-cAMP (cAMP) also mimicked the antimigratory effects of NO donors, the antimigratory effects of SNAP were not altered by 2',5'-dideoxyadenosine (an inhibitor of adenyl cyclase) or by (R)-p-adenosine-3',5'-cyclic phosphorothioate (an inhibitor of the cAMP-dependent protein kinase). Low concentrations of the subtype AT1-receptor antagonist CGP 48933, but not the subtype AT2-receptor antagonist CGP 42112, blocked AII-induced SMC migration. These findings indicate that (a) NO inhibits AII-induced migration of vascular SMCs; (b) the antimigratory effect of NO is mediated in part via a cGMP-dependent mechanism; and (c) AII stimulates SMC migration via an AT1 receptor.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2001

Stimulation of human extravillous trophoblast migration by IGF-II is mediated by IGF type 2 receptor involving inhibitory G protein(s) and phosphorylation of MAPK.

We have earlier shown that migration and invasiveness of first trimester human extravillous trophoblast cells are stimulated by IGF-II, independently of IGF type 1 receptor and that migration stimulation is the primary reason for increased extravillous trophoblast cell invasiveness induced by IGF-II. In the present study we examined the functional role of IGF type II receptor in IGF-II stimulation of extravillous trophoblast cell migration and the underlying signal transduction pathways including the participation of inhibitory G protein(s) and MAPK. The migratory ability of a well characterized in vitro propagated human first trimester extravillous trophoblast cell line expressing the phenotype of extravillous trophoblast cells in situ was quantitated with a Transwell migration assay under different experimental conditions. We found that the extravillous trophoblast cells expressed an abundance of IGF type 2 receptor as detected by immunostaining and Western blots, and recombinant human IGF-II promoted their migration in a dose- and time-dependent manner. Both polyclonal and monoclonal IGF type 2 receptor-blocking antibodies blocked migration-stimulating effects of IGF-II. Two synthetic IGF-II analogs ([Leu27]IGF-II, which can bind to IGF type 2 receptor and IGF-binding proteins, but not IGF type 1 receptor, and [QAYL-Leu27]IGF-II, which can bind to IGFR-II, but neither IGFR-I nor IGF-binding proteins) both stimulated extravillous trophoblast cell migration to levels higher than those induced by wild-type IGF-II. These results reveal that IGF-II action was mediated by IGF type 2 receptor, independently of IGF type 1 receptor and IGF-binding proteins. Treatment of extravillous trophoblast cell membrane preparations with IGF-II decreased adenylyl cyclase activity in a concentration-dependant manner, indicating the participation of inhibitory G proteins in IGF-II action. This was substantiated further with the findings that increasing intracellular cAMP using forskolin or (Bu)2cAMP inhibited basal extravillous trophoblast cell migration and blocked IGF-II stimulation of migration. IGF-II treatment rapidly stimulated phosphorylation of MAPK (ERK-1 and -2), which was blocked by pretreatment of extravillous trophoblast cells with the MAPK kinase (MEK) inhibitor PD98059. Treatment with this inhibitor also blocked extravillous trophoblast cell migration in the presence or absence of IGF-II. These results, taken together, reveal that IGF-II stimulates extravillous trophoblast cell migration by signaling through IGF type 2 receptor, involving inhibitory G proteins and activating the MAPK pathway.

Adenylyl Cyclases↗
PubMed2005

Slow muscle regulates the pattern of trunk neural crest migration in zebrafish.

In avians and mice, trunk neural crest migration is restricted to the anterior half of each somite. Sclerotome has been shown to play an essential role in this restriction; the potential role of other somite components in specifying neural crest migration is currently unclear. By contrast, in zebrafish trunk neural crest, migration on the medial pathway is restricted to the middle of the medial surface of each somite. Sclerotome comprises only a minor part of zebrafish somites, and the pattern of neural crest migration is established before crest cells contact sclerotome cells, suggesting other somite components regulate the pattern of zebrafish neural crest migration. Here, we use mutants to investigate which components regulate the pattern of zebrafish trunk neural crest migration on the medial pathway. The pattern of trunk neural crest migration is aberrant in spadetail mutants that have very reduced somitic mesoderm, in no tail mutants injected with spadetail morpholino antisense oligonucleotides that entirely lack somitic mesoderm and in somite segmentation mutants that have normal somite components but disrupted segment borders. Fast muscle cells appear dispensable for patterning trunk neural crest migration. However, migration is abnormal in Hedgehog signaling mutants that lack slow muscle cells, providing evidence that slow muscle cells regulate the pattern of trunk neural crest migration. Consistent with this idea, surgical removal of adaxial cells, which are slow muscle precursors, results in abnormal patterning of neural crest migration; normal patterning can be restored by replacing the ablated adaxial cells with ones transplanted from wild-type embryos.

Animals↗
PubMed1995

Segmental migration of trunk neural crest: time-lapse analysis reveals a role for PNA-binding molecules.

Trunk neural crest cells migrate through the somites in a striking segmental fashion, entering the rostral but not caudal sclerotome, via cues intrinsic to the somites. Attempts to define the molecular bases of these cues have been hampered by the lack of an accessible assay system. To examine trunk neural crest migration over time and to perturb candidate guiding molecules, we have developed a novel explant preparation. Here, we demonstrate that trunk regions of the chicken embryo, placed in explant culture, continue to develop apparently normally for 2 days. Neural crest cells, recognized by prelabeling with DiI or by poststaining with the HNK-1 antibody, migrate in the somites of the explants in their typical segmental pattern. Furthermore, this paradigm allows us to follow trunk neural crest migration in situ for the first time using low-light-level videomicroscopy. The trajectories of individual neural crest cells were often complex, with cells migrating in an episodic mode encompassing forward, backward and lateral movements. Frequently, neural crest cells migrated in close-knit groups of 2-4 cells, moving at mean rates of migration of 10-14 microns/hour. Treatment of the explants with the lectin peanut agglutinin (PNA) both slowed the rate and altered the pattern of neural crest migration. Neural crest cells entered both the rostral and caudal halves of the sclerotome with mean rates of migration ranging from 6 to 13 microns/hour. These results suggest that peanut agglutinin-binding molecules are required for the segmental patterning of trunk neural crest migration. Because this approach permits neural crest migration to be both observed and perturbed, it offers the promise of more direct assays of the factors that influence neural crest development.

Animals↗
PubMed2005

Cyclic AMP mediates keratinocyte directional migration in an electric field.

Re-epithelialization of wounded skin is necessary for wound closure and restoration of barrier function and requires directional keratinocyte migration towards the center of the wound. The electric field (EF) generated immediately upon wounding could be the earliest signal keratinocytes receive to initiate directional migration and healing. Keratinocytes express many beta2-adrenergic receptors (beta2-ARs), but their role in the epidermis is unknown. We have previously shown that beta-AR agonists decrease keratinocyte migration in a cyclic AMP (cAMP) independent mechanism involving the activation of protein phosphatase 2A (PP2A). Here, we ask whether beta2-ARs play a role in keratinocyte galvanotaxis. We report a bimodal response. When keratinocytes were exposed to higher concentrations of beta-AR agonist (0.1 microM), their tracked migratory speed was inhibited, in both the presence (directional migration) and the absence (random migration) of a 100 mV mm(-1) EF, as expected. At lower agonist concentrations (0.1 pM to 0.1 nM), there was no effect on migratory speed; however, all directionality was lost - essentially, cells were 'blinded' to the directional cue. Preincubating the cells with beta-antagonist restored directional migration, demonstrating that the 'blindness' was beta2-AR mediated. Incubation of keratinocytes with agents known to increase intracellular cAMP levels, such as sp-cAMP, pertussis toxin and forskolin, resulted in similar 'blinding' to the EF, whereas random migration was unaffected. The inactive cAMP analog rp-cAMP had no effect on keratinocyte migration, whether directional or random. However, rp-cAMP pretreatment before beta-agonist addition fully restored galvanotaxis, demonstrating the complete cAMP dependence of the attenuation of keratinocyte directional migration. This is the first report that cAMP is capable of mediating keratinocyte galvanotaxis. beta-AR agonists and antagonists could be valuable tools for modulating re-epithelialization, an essential step in the wound-healing process. Thus, beta-ARs regulate the two distinct components of keratinocyte directional migration differently: migration speed via a cAMP-independent mechanism and galvanotaxis by a cAMP-dependent one.

Adenylyl Cyclases↗
PubMed1999

Epidermal growth factor receptor relocalization and kinase activity are necessary for directional migration of keratinocytes in DC electric fields.

Human keratinocytes migrate towards the negative pole in DC electric fields of physiological strength. This directional migration is promoted by epidermal growth factor (EGF). To investigate how EGF and its receptor (EGFR) regulate this directionality, we first examined the effect of protein tyrosine kinase inhibitors, including PD158780, a specific inhibitor for EGFR, on this response. At low concentrations, PD158780 inhibited keratinocyte migration directionality, but not the rate of migration; at higher concentrations, it reduced the migration rate as well. The less specific inhibitors, genistein, lavendustin A and tyrphostin B46, reduced the migration rate, but did not affect migration directionality. These data suggest that inhibition of EGFR kinase activity alone reduces directed motility, and inhibition of multiple tyrosine kinases, including EGFR, reduces the cell migration rate. EGFR redistribution also correlates with directional migration. EGFR concentrated on the cathodal face of the cell as early as 5 minutes after exposure to electric fields. PD158780 abolished EGFR localization to the cathodal face. These data suggest that EGFR kinase activity and redistribution in the plasma membrane are required for the directional migration of keratinocytes in DC electric fields. This study provides the first insights into the mechanisms of directed cell migration in electric fields.

Cell Movement↗
PubMed1999

Hyaluronan stimulates tumor cell migration by modulating the fibrin fiber architecture.

The glycosaminoglycan hyaluronan, which supports tumor cell migration and metastasis, interferes with fibrin polymerization and leads to increased fiber size and porosity of fibrin clots. Here we have studied the proportionate effect of fibrin polymerization on hyaluronan-mediated migration of glioblastoma cells. The structural and physical properties of hyaluronan-containing fibrin gels were analyzed by turbidity measurement, laser scanning microscopy, compaction assay, and calculation of pore size by liquid permeation. When fibrin polymerized in the presence of hyaluronan or dextran, the resulting gels strongly stimulated cell migration, and migration significantly correlated with fiber mass-to-length ratios and pore diameters. In contrast, cell migration was not induced by addition of hyaluronan to supernatants of already polymerized gels. Hyaluronan-mediated migration was inhibited in fibrin gels by antibodies to alphav- and beta1integrins and the disintegrin echistatin, but not by antibodies to the hyaluronan receptor CD44 (up to 50 microg/ml). As a control, we show that anti-CD44 (10 microg/ml) inhibited cell migration on a pure hyaluronan matrix using a two-dimensional Boyden chamber system. In contrast to three-dimensional migration, the migration of cells on the surfaces of variably structured fibrin gels was not significantly different, indicating that increased gel permeability (porosity) may account for hyaluronan-mediated migration. We conclude that, in complex three-dimensional substrates, the predominant effect of hyaluronan on cell migration might be indirect and requires modulation of fibrin polymerization.

Animals↗
PubMed1981

Inverse correlation between neutrophil microtubule numbers and enhanced random migration.

The random migration of neutrophils under agarose as measured by the number of cells leaving the well, is enhanced when the pH or the osmolality of the medium is reduced or when microtubule agents are used. Concentrations of colchicine above 5 x 10-7 M increased the number of cells migrating and decreased the mean number of centriolar microtubules in a dose-dependent fashion from 16 to 4 per 4 micron 2 at 10-5 M. The distance that colchicine-treated neutrophils migrated from the well was not different from the control. Lowering the pH from 7.4 to 6.0 also increased random migration and decreased pericentriolar microtubules from a mean of 16 to a mean of 10. At pH 6.0, both the number of cells that migrated and the distance the cells forming the leading edge travelled from the well were increased. Since peripheral microtubules may play a greater role in cell migration than centiolar ones, we examined the numerical density of microtubules in the peripheral cytoplasm. Lowering the medium pH reduced the mean number of microtubules per 10 micron 2 from 6 to 2. Colchicine reduced micro-tubules in the same area to I. At the low pH, colchicine reduced even further the numbers of both centriole-associated and peripheral microtubules but the migration pattern was the same as that seen at pH 6.0 without colchicine. Lowering medium osmolality from 280 to 230 m-osmol increased random migration but did not affect microtubule numbers. The addition of colchicine to this system decreased microtubule numbers and increased migration even further. Conditions that enhanced neutrophil migration also affected cell shape. Whereas cells at pH 7.4 were generally fan-shaped with a broad, smooth leading edge, cells at pH 6.0 with or without colchicine were long and narrow. Neutrophils at pH 7.4 but 230 m-osmol had a scalloped edge, which often appeared thickened. This too was not altered by colchicine. The morphology of cells treated with colchicine was similar to controls except for the more frequent presence of long retraction fibres. Each of these treatments thus appears to act on a different aspect of the cell's locomotory apparatus. The mechanisms by which colchicine and lowered ph enhance migration may partially overlap since both significantly decrease peripheral microtubules. The data suggest that microtubules play a constraining role within the cell, limiting the ability of the cell to move and change direction.

Adult↗
PubMed1988

Newt epidermal cell migration over collagen and fibronectin involves different mechanisms.

Effects of the synthetic peptides, Arg-Gly-Asp-Ser (RGDS), the amino acid sequence representing the fibroblast attachment site in fibronectin, and Arg-Gly-Glu-Ser (RGES), on collagen- and fibronectin-mediated migration in newt epidermal cells were compared. When RGDS at 50 micrograms ml-1 was included in the incubation medium of skin explants, migration in fibronectin-coated dishes was almost totally blocked. In type I collagen-coated dishes, this concentration of RGDS also inhibited migration, but to a lesser degree than on fibronectin. With 250 micrograms ml-1 of RGES in the medium, the reverse was true. Here, migration on collagen was practically non-existent, while migration on fibronectin was affected only moderately. Collagen-mediated migration was sensitive to RGDS even when the peptide was added after migration on the coated substratum was well underway. At a coating concentration of 10 micrograms ml-1 CB3, a cyanogen bromide fragment of the collagen alpha 1(I) chain, which contains no RGD sequences, was as good a migration substratum as intact collagen applied at the same coating concentration. At lower concentrations intact collagen was somewhat better than equivalent concentrations of CB3. The presence of RGDS in the medium throughout an experiment inhibited migration in CB3-coated dishes in a manner similar to its effect in dishes coated with collagen. On both substrata there appeared to be a peptide-sensitive and a peptide-insensitive component to migration. The inhibitory effect of RGES on CB3-mediated migration was also similar to its effect in collagen-coated dishes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Binding of lectins to novel migration promoters on cardiac mesenchymal cells in the chick.

Chicken serum promotes migration of cardiac mesenchymal cells of chick embryos in vitro. In the present study, migration promotion of unknown migration promoters in chicken serum was examined by using lectins. Cardiac mesenchymal cells of the conotruncal and atrioventricular cushions were cultured on collagen type-I gel with medium including chicken serum. A concentration (100 micrograms/ml) of Concanavalin A (Con A), peanut agglutinin (PNA), pisum sativum agglutinin (PSA), soybean agglutinin (SBA) or wheat germ agglutinin (WGA) was added to the medium. Con A, PSA, and WGA inhibited migration, while PNA and SBA did not affect migration of cardiac mesenchymal cells. WGA inhibited migration in a concentration dependent manner. Preincubation of WGA with specific binding monosaccharides (alpha-D-N-acetylglucosamine and alpha-D-N-acetylneuraminic acid) clearly reduced the inhibition ability of WGA, while preincubation of Con A and PSA with alpha-D-mannose and alpha-D-glucose did not. On the other hand, Con A-binding proteins, eluted from a Con A affinity column with the buffer including alpha-D-mannose and alpha-D-glucose, promoted migration of cardiac mesenchymal cells, as did WGA-binding proteins. These proteins promoted migration in a concentration dependent manner. Western blotting showed that PSA bound the subunits of collagen type-I, but ConA and WGA did not. In migration inhibition assays by monosaccharides, only N-acetylneuraminic acid inhibited migration of cardiac mesenchymal cells. These results suggested that chicken serum contains novel migration promoters for chick cardiac mesenchymal cells. The promoters are proposed to have the terminal N-acetylglucosamine, N-acetylneuraminic acid, and glucose and/or mannose residues.

Animals↗
PubMed2006

Increased migration of vascular adventitial fibroblasts from spontaneously hypertensive rats.

Experimental evidence has suggested that vascular adventitial fibroblasts (AFs) may migrate into the neointima of arteries after balloon injury in various animal models. However, the research on migration of AFs has been limited to the effects of acute vascular injury. The role of AFs in chronic vascular injury and hypertension is not yet known. In this study, the migration of spontaneously hypertensive rat (SHR)-AFs and Wistar-Kyoto rat (WKY)-AFs from the thoracic aorta was determined by a transwell technique. Our results showed that fetal calf serum, angiotensin II (Ang II), phorbol ester, basic fibroblast growth factor and platelet-derived growth factor-BB induced migration in a dose-dependent manner, and the migration of SHR-AFs was always greater than that of WKY-AFs. Ang II-induced migration of AFs was considered to have been mediated by Ang II type 1 receptor (AT1-R), because the AT1-R antagonist losartan (10(-7)-10(-5) mol/l) suppressed Ang II-induced migration. Ang II-induced migration was also blocked by the extracellular-regulated protein kinase 1/2 (ERK1/2) inhibitor PD98059 (10(-5) mol/l) and p38 kinase inhibitor SB202190 (10(-5) mol/l), indicating that ERK1/2 and p38 kinase were involved in Ang II-induced migration. Ang II (10(-7) mol/l)-induced ERK1/2 and p38 kinase phosphorylation, both of which peaked after 5 min, were suppressed by PD98059 and SB202190, respectively. The Ang-II induced phosphorylation of both proteins was suppressed by losartan, whereas no effect was observed with PD123319, a specific inhibitor of Ang II type 2 receptor (AT2-R). Thus, in the present study, various factors stimulated the migration of SHR-AFs and, to a leber extent, WKY-AFs from the thoracic aorta, and the ERK1/2 and p38 kinase pathways are involved in Ang II-stimulated migration of fibroblasts.

Angiotensin II↗
PubMed2005

Temporal and spatial variation in age-specific net migration in the United States.

As fertility differences in the United States diminish, population redistribution trends are increasingly dependent on migration. This research used newly developed county-level age-specific net migration estimates for the 1990s, supplemented with longitudinal age-specific migration data spanning the prior 40 years, to ascertain whether there are clear longitudinal trends in age-specific net migration and to determine if there is spatial clustering in the migration patterns. The analysis confirmed the continuation into the 1990s of distinct net migration "signature patterns" for most types of counties, although there was temporal variation in the overall volume of migration across the five decades. A spatial autocorrelation analysis revealed large, geographically contiguous regions of net in-migration (in particular, Florida and the Southwest) and geographically contiguous regions of net out-migration (the Great Plains, in particular) that persisted over time. Yet the patterns of spatial concentration and fragmentation over time in these migration data demonstrate the relevance of this "neighborhood" approach to understanding spatiotemporal change in migration.

Adolescent↗
PubMed1999

Cohort migration of carcinoma cells: differentiated colorectal carcinoma cells move as coherent cell clusters or sheets.

Active migration of tumor cells is usually assessed as single cell locomotion in vitro using Boyden chamber-type assays. In vivo, however, carcinoma cells, malignant cells of epithelial origin, frequently invade the surrounding tissue as coherent clusters or nests of cells. We have called this type of movement "cohort migration". In our work, the invasion front of colon carcinomas consisted of compact tumor glands, partially resolved glands or markedly resolved glands with scattered tumor cell clusters or single cells lying ahead. In the former two types, which constituted about a half of all cases, cohort migration seems to be the predominant mechanism, whereas both cohort migration and single cell locomotion may be involved in the last one. In this light, it is very advantageous to investigate the mechanisms involved in the cohort migration. In this review, we present a two-dimensional motility assay as a cohort migration model, in which human colorectal carcinoma cells move outwards from the cell islands mainly as localized coherent sheets of cells when stimulated with 12-O-tetradecanoylphorbol-13-acetate (TPA) or hepatocyte growth factor/scatter factor (HGF/SF). Within the migrating cell sheets, wide intercellular gaps occur at the lower portion of the cells to allow the cells to extend leading lamellae forward while close cell-cell contacts remain at the upper portion of the cells. This localized modulation of cell-cell adhesion at the lower portion of the cells is associated with increased tyrosine phosphorylation of the E-cadherin-catenin complex in TPA-induced cohort migration and with reduced alpha-catenin complexed with E-cadherin in HGF/SF-induced cohort migration. Furthermore, fibronectin deposited by migrating cells is essential for their movement, and on the gelatin-coated substrate even degradation and remodeling of the substrate by matrix metalloproteinases are also needed. Thus, in cohort migration it is likely that cells are released from cell-cell adhesion only at the lower portion of the cells via modulation of E-cadherin-catenin-based mechanism, and this change allows the cells to extend leading lamellae onto the extracellular matrix substrate remodeled by deposition of fibronectin and organized digestion.

Animals↗
PubMed2004

GABA release and uptake regulate neuronal precursor migration in the postnatal subventricular zone.

In the postnatal subventricular zone (SVZ), astrocyte-like cells tightly encapsulate chains of migrating neuronal precursors, although an influence of the astrocyte-like cells on precursor migration has not yet been demonstrated. Cell migration was studied in acute sagittal brain slices to determine whether GABA signaling between astrocyte-like cells and neuronal precursors controls the speed of neuronal precursor migration in the anterior SVZ and rostral migratory stream of juvenile and adult mice. Application of GABA at 10 microm, a nondesensitizing concentration for GABA(A) receptors (GABA(A)Rs), reduced the rate (mean of approximately 50 microm/hr) of cell migration by 21% via GABA(A)R activation. Application of the GABA(A)R antagonist bicuculline enhanced the migration rate by 30%, suggesting that endogenous GABA tonically reduces the speed of cell migration via GABA(A)R activation. Using immunohistochemistry, we found that astrocyte-like cells express the high-affinity GABA transporter subtype GAT4 on processes ensheathing neuronal precursors that contain GABA. Inhibition of GABA uptake into astrocyte-like cells or enhancement of GABA release from neuronal precursors during high K(+) application further reduced the migration rate by increasing ambient GABA levels. GABA altered the migration speed by interfering with intracellular Ca(2+) signaling independently of cell depolarization, because high K(+) application did not alter the speed of cell migration in the presence of bicuculline. These data indicate that astrocyte-like cells create a microenvironment in which their uniquely positioned GABA transporters control the degree of GABA(A)R activation and the migration of neuronal precursors.

Animals↗
PubMed2000

Adhesion molecules involved in transendothelial migration of human hematopoietic progenitor cells.

In the process of homing, CD34(+) hematopoietic progenitor cells migrate across the bone marrow endothelium in response to stromal cell-derived factor (SDF)-1. To develop more efficient stem cell transplantation procedures, it is important to define the adhesion molecules involved in the homing process. Here, we identified the adhesion molecules that control the migration of primary human CD34(+) cells across human bone marrow endothelial cells. Migration of CD34(+) cells is enhanced across interleukin 1beta prestimulated bone marrow endothelium, suggesting an important role for the endothelium in adhesion and formation of the chemotactic gradient. Under these conditions, 30-100 ng/ml SDF-1 induced a rapid and efficient migration of CD34(+) cells (+/- 46% migration in 4 h). In contrast, 600-1,000 ng/ml SDF-1 were required for optimal migration across fibronectin-coated filters. Subsequent studies revealed that transendothelial migration of CD34(+) cells is mediated by beta1- and beta2-integrins and PECAM-1 (CD31) but not by CD34 or E-selectin. Whereas these antibodies individually blocked migration for 25%-35%, migration was reduced by 68% when the antibodies were combined. Thus, these adhesion molecules play specific and independent roles in the transmigration process. Finally, O-glycosylated proteins appeared to play a role, since SDF-1-induced migration of CD34(+) cells (treated with a glycoprotease from Pasteurella haemolytica) across endothelial cells was clearly inhibited. In conclusion, we show that efficient SDF-1-induced migration of primary human CD34(+) cells across bone marrow endothelium is mediated by beta1-integrins, beta2-integrins, CD31 and O-glycosylated proteins.

Antigens, CD↗
PubMed1985

Stimulatory effect of insulin on aortic smooth muscle cell migration induced by 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid and its modulation by elevated extracellular glucose levels.

In investigations on the role of insulin on migration of rat aortic smooth muscle cells, migration of the cells was measured by a modified Boyden chamber technique with 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE) as a chemoattractant. Insulin itself was not a chemoattractant for these cells, and insulin added just before the migration assay did not affect cell migration in the presence or absence of 12-HETE. Cells pretreated with insulin in culture dishes for a long period, however, showed a significant increase in migration induced by 12-HET, and the increase depended on the insulin concentration: concentrations of insulin of greater than 50 microIU/ml caused about twofold increase in cell migration. On the other hand, long-term incubation with various concentrations of insulin (0.15-1000 microIU/ml) did not affect nonspecific cell migration in the absence of 12-HETE. The stimulatory effect of insulin on cell migration gradually increased with the duration of insulin treatment, reaching a plateau after 4 days. Thus, insulin stimulated 12-HETE-induced smooth muscle cell migration in a time- and dose-dependent manner. When the extracellular D-glucose concentration in the Boyden chamber was increased from 100 to 300 mg/dl, the stimulatory effect of insulin on 12-HETE-induced cell migration was augmented. This modulation by D-glucose was not due to an increase in the osmotic pressure of the medium, since addition of mannitol to increase the osmotic pressure did not enhance the effect of insulin on cell migration.(ABSTRACT TRUNCATED AT 250 WORDS)

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1987

Indirect food additive migration from polymeric food packaging materials.

Many foods contact polymeric packaging materials which contain residues of the polymerization process or additives employed to facilitate processing. The extent of migration of such materials from the packaging to foods is the focus of the present article. A major experimental program using eight polymer-migrant systems is described. Migration was measured to food-simulating liquids (FSL) and to foods. Accelerated tests were conducted with FSL under FDA guidelines conditions so as to develop correlations between such data and those found using foods under normal storage temperatures and shelf lives. In the majority of tests, the migration was found to be approximately proportional to the square root of time, to increase significantly with a rise in temperature, and to be proportional to the initial concentration of migrant in the polymer. Stirring in the FSL or food phase was generally not important except for the system involving dioctyl adipate migrating from polyvinyl chloride film. In some instances, after a period of time, migration rates became very low, and this effect was attributed to saturating the FSL or food phase with migrant. The foods comprised a variety of types, including liquid, semisolid, solid, and dry; both oily and aqueous foods were included. The physical steps involved in migration include the diffusion of the migrant from the interior of the film to the surface, where it can dissolve in the external FSL or food phase. The nature of the FSL or food is shown to be very important in that components can penetrate the polymer and dramatically increase migration rates. Consistent with the FDA guidelines in effect at the time of this study, testing was performed with five FSL (water, 3% acetic acid, 8% and 50% ethanol, and n-heptane) at 49 degrees C. Detailed comparisons were made between the migrations to foods and to FSL; following are the more relevant conclusions. (1) Three percent acetic acid showed no advantage over water as a food simulant even in those cases where the food could be considered acidic in nature. (2) Water, when used as an FSL at 49 degrees C for 5 days, overestimated migration in aqueous foods in about 75% of the cases. In some instances, however, the water phase became saturated with migrant. In other situations, this test protocol underpredicted migration--especially in those cases where there were components in the food that were able to penetrate into the polymer and enhance migration (such as orange juice).(ABSTRACT TRUNCATED AT 400 WORDS)

Chemical Phenomena↗