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PubMed1998

Integrins, cell matrix interactions and cell migration strategies: fundamental differences in leukocytes and tumor cells.

The principles determining the migration of different cell types may results from their differences in origin, size and shape, function of adhesion receptors, and environmental factors, including the extracellular matrix. Polarized leukocytes (T lymphocytes and dendritic cells) migrating in three-dimensional collagen lattices are small developing a highly dynamic leading edge and a trailing uropod, whereas invasive melanoma cells are larger, highly polarized and less dynamic. In contrast to leukocyte, tumor cells may additionally develop migrating cell clusters maintaining intense cell-cell interaction and cluster polarity. Leukocytes show a speed-oriented, oscillating and directionally unpredictable path profile strongly guided by matrix fibers, while melanoma cells and migrating cell clusters exhibit slow yet highly directional migration. Whereas leukocytes form short-lived interactions with collagen fibers in complete absence of tissue remodeling, melanoma cells and neoplastic cell clusters reorganize the matrix via profound pulling at attachment sites, limited fiber disruption upon detachment, and the shedding of cell surface determinants. Using blocking anti-integrin antibodies, tumor cell migration and migration-associated matrix reorganization were shown to be dependent on beta 1 integrin-mediated adhesion, whereas migrating T cells cannot be inhibited by a panel of anti-beta 1-, beta 2-, beta 3-, and alpha-integrin antibodies, either alone or in combination. Consequently, migrating melanoma cells use focal adhesions of integrins coclustered with cytoskeletal components at contacts with collagen fibers. T cells, however, lack typical focal adhesions, redistribute beta 1 integrins to the uropod and the focal adhesion kinase to the leading edge. In conclusion, an adhesion-dependent and reorganizing migration type employed by melanoma cells may be distinct from largely integrin-independent and non-reorganizing migration strategies used by leukocytes.

Cell Movement↗

PubMed1999

Meloxicam effect on leukocyte migration under shear stress: a new perfused triple chamber (Hofbauer chamber) assay simulating an in vitro vascular wall.

BACKGROUND: Leukocyte migration plays a tremendous role during inflammation. Different drugs are able to influence migration of leukocytes. Several authors have attempted to establish methods for investigation of leukocyte migration. Migration of leukocytes under conditions simulating natural blood flow and shear stress is poorly understood. Moreover, leukocyte migration in the simultaneous presence of endothelial cells and smooth muscle cells (SMC) has not yet been examined thoroughly. The aim of the current study was to create a new three-dimensional assay investigating migration during simulated perfusion. The assay was used for investigating the effect of meloxicam on leukocyte migration under shear stress. METHODS: Different concentrations of meloxicam (0.09, 0.9, and 9.0 ng/mL) were used in a newly developed triple migration chamber system for investigation of leukocyte migration (n = 7). This new system allows inclusion of SMC-layers. Assay precision tests were done using intra-assay (within-day variability) and interassay (day-to-day variability) controls. RESULTS: Intra-assay and interassay controls showed reliable results (coefficient of variation: intra-assay 8.53%; interassay 11.39%). Meloxicam in a clinically relevant concentration of 0.9 ng/mL was able to reduce the migration of leukocytes under shear stress (71 +/- 14% SD; P < 0.05), whereas higher and lower concentrations showed a dose dependent effect. CONCLUSION: This new perfusion system allows investigation of drugs, such as meloxicam, on leukocyte migration under shear stress. Moreover, this assay may be used for studies on other cell-cell interactions, as well as on drug influences.

Adult↗

PubMed2000

Secreted phospholipase A(2) induces vascular endothelial cell migration.

Secreted phospholipase A(2) (sPLA(2)) regulates a variety of cellular functions. The present investigation was undertaken to elucidate the potential role of sPLA(2) in endothelial cell (EC) migration. Bovine aortic endothelial cells (BAECs) exposed to sPLA(2) placed in the lower compartment of a modified Boyden chamber displayed increased migration compared to cells exposed to vehicle. The effect of sPLA(2) on EC migration was time and dose dependent. Migration of BAECs was observed at 30 minutes, increased over 1 to 2 hours, and declined thereafter. At 2 hours of stimulation, sPLA(2) (0.01-2 micromol/L) induced 1.2- to 3-fold increased cell migration compared with media alone. Among the different sPLA(2)s tested, bee venom, Naja naja, and porcine and human pancreatic PLA(2)s all evoked a migratory response in ECs. Moreover, human synovial fluid, obtained from patients with arthritis and containing sPLA(2) activity, induced EC migration. Migration of ECs was significantly reduced after exposure to a catalytic site mutant of pancreatic sPLA(2) with decreased lipolytic activity as compared to wild-type sPLA(2). Similarly, pretreatment of human synovial fluid with p-bromophenacyl bromide, an irreversible inhibitor of sPLA(2), markedly decreased the ability of human synovial fluid to stimulate EC migration. Moreover, migration of ECs was stimulated on exposure to hydrolytic products of sPLA(2) activity including arachidonic acid, lysophosphatidic acid, and lysophosphatidylcholine. These findings suggest that sPLA(2) plays a physiologic role in induction of EC migration. Moreover, the effects of sPLA(2) on EC migration are mediated, at least in part, by its catalytic activity. (Blood. 2000;96:3809-3815)

Amino Acid Substitution↗

PubMed2002

Polyamine-dependent migration of retinal pigment epithelial cells.

PURPOSE: Migration of retinal pigment epithelial (RPE) cells can be triggered by disruption of the RPE monolayer or injury to the neural retina. Migrating cells may re-establish a confluent monolayer, or they may invade the neural retina and disrupt visual function. The purpose of this study was to examine the role of endogenous polyamines in mechanisms of RPE migration. METHODS: Endogenous polyamine levels were determined in an immortalized RPE cell line, D407, using HPLC. Activities of the two rate-limiting enzymes for polyamine synthesis, ornithine decarboxylase (ODC), and S-adenosylmethionine decarboxylase (SAMdc), were measured by liberation of ((14)CO(2))(.) Migration was assessed in confluent cultures by determining the number of cells migrating into a mechanically denuded area. All measurements were obtained both in control cultures and in cultures treated with synthesis inhibitors that deplete endogenous polyamines. Subcellular localization of endogenous polyamines was determined using a polyamine antibody. RESULTS: The polyamines, spermidine and spermine, as well as their precursor, putrescine, were normal constituents of RPE cells. The two rate-limiting synthetic enzymes were also present, and their activities were stimulated dramatically by addition of serum to the culture medium. Cell migration was similarly stimulated by serum exposure. When endogenous polyamines were depleted, migration was blocked. When polyamines were replenished through uptake, migration was restored. Polyamine immunoreactivity was limited to membrane patches in quiescent cells. In actively migrating and dividing cells, immunoreactivity was enhanced throughout the cytoplasm. CONCLUSIONS: Polyamines are essential for RPE migration. Pharmacologic manipulation of the polyamine pathway could provide a therapeutic strategy for regulating anomalous migration.

Adenosylmethionine Decarboxylase↗

PubMed1986

Macrophage migration in fibrin gel matrices.

Macrophage migration has been extensively studied in vitro on artificial substrates but in vivo macrophages migrate through connective tissue and fibrin gel meshworks that comprise the stroma of many inflammatory reactions and solid tumors. Studies were therefore undertaken to investigate macrophage migration in this more biologically relevant matrix cast either with or without nitrocellulose filter support. Macrophage migration in fibrin gels depended on both fibrin and thrombin concentrations and on the nature of fibrin crosslinking. With gamma-chain crosslinking only, macrophage migration was enhanced as compared with untreated filters at fibrin concentrations of up to 5 mg/ml. However, when fibrin alpha-chains were also crosslinked, as occurs in vivo, macrophage migration was inhibited at approximately 3 mg/ml fibrin and was stopped altogether at 5 mg/ml. Thrombin concentrations of 1 unit/ml favored maximal macrophage migration. Depletion of contaminating fibronectin did not affect these results. The pore size of fibrin gels is well below the minimum that permits macrophage migration through nitrocellulose filters. Thus, to penetrate fibrin gels, macrophages could enlarge effective pore size by local fibrinolysis or by pushing apart fibrin strands. If fibrinolysis is responsible, this process must be highly localized because only small amounts of fibrinolysis accompanied extensive macrophage migration in fibrin gels; moreover, fibrinolysis inhibitors did not affect macrophage migration. We conclude that the fibrin deposited in inflammatory reactions and solid tumors is present in forms and concentrations that either facilitate or inhibit macrophage migration; fibrin may therefore regulate macrophage participation in these and other pathologic reactions.

Animals↗

PubMed1985

Variations in interstate migration of men across the early stages of the life cycle.

The results reported here show that the stage of an individual's life cycle not only has direct effects on the likelihood of migration, but also establishes a context within which the motives to migrate are evaluated and acted upon. One contextual impact of the life cycle concerns the effects of length of residence on migration. The results show that the probability of migrating declines more rapidly over time for married males with children than for singles males--i.e., the difference between the likelihood of migration for single males and married males with children widens with increasing length of residence. Much of this difference may be due to the greater number and strength of community ties for individuals who are married with children. These ties are not well developed at the beginning of a residence but continue to strengthen over the course of a residence. In addition, there are variations in the levels of job rewards and location-specific resources across the life cycle and there are two variations across the early life cycle in the effects of independent variables on the initial rate of migration. One resource (self-employment) and one job reward (prestige) have different effects for single individuals than for either group of married males. If the span of the life cycle considered in this analysis were broadened to include older men, additional differences in the effects of independent variables might be uncovered. In research with cross-sectional data containing a wider range of ages than the data used here, Heaton et al. (1981) found that economic variables were more important in determining the migration of younger individuals than that of older individuals, whereas noneconomic factors were more important determinants of the migration of older than of younger individuals. The results of this paper and Heaton's results suggest that at different stages of life people use a somewhat different "subjective cost-benefit calculus" in making migration decisions. The importance of certain migration determinants may vary significantly depending on whether an individual is married, whether he or she has children, and/or whether he or she is in the labor force or retired. Additional research on these issues could greatly contribute to our understanding of migration.

Adult↗

PubMed1985

The influence of antiplatelet drugs on injury-stimulated migration of cultured smooth muscle cells.

Smooth muscle cell (SMC) migration, one of the early events in arteriosclerotic lesion formation in vivo, can be triggered by balloon catheter injury. This accelerated migration persists when aortic explants are grown in tissue culture. Under low serum conditions (0.1% fetal bovine serum) virtually no smooth muscle cell migration occurs out of explants from sham operated control animals, while over 70% of explants from balloon injured rats show SMC migration. Since platelets are thought to contribute to SMC proliferation and migration, we tested the effect of different antiplatelet drugs (sulfinpyrazone, aspirin, dipyridamole, and a combination of the last two) on balloon injury stimulated SMC migration. One week after onset of drug treatment balloon catheterization was performed and SMC migration from aortic explants was assessed 4 days later in vitro. The time and number of explants showing SMC migration was recorded daily over 8 days. Sulfinpyrazone reduced stimulated SMC migration most effectively, followed by the combination of aspirin and dipyridamole, while aspirin or dipyridamole alone had no significant effect on stimulated SMC migration. Using this technique we were able to single out SMC migration and analyze the effect of antiplatelet drugs on this early step in arteriosclerotic lesion formation.

Animals↗

PubMed1983

Enteric mechanisms of initiation of migrating myoelectric complexes in dogs.

The enteric mechanisms governing initiation of migrating myoelectric complexes were studied in 6 conscious dogs, each implanted with a set of 12 bipolar electrodes on the small intestine. The small intestine was transected and reanastomosed at three sites to give four isolated segments of equal length. Each segment had three implanted electrodes. All four isolated segments generated migrating myoelectric complexes which were, initially, totally independent of each other in time. The most proximal segment had the longest mean migrating myoelectric complex time period (106.2 +/- 10.1 SEM min) and the second segment had the shortest mean migrating myoelectric complex time period (66.8 +/- 6.7 SEM min). Distal to the second segment, the mean migrating myoelectric complex time period increased progressively (83.1 +/- 11.2 SEM min and 95.8 +/- 7.6 SEM min, respectively). Isolation of the small intestine into segments did not significantly change migrating myoelectric complex propagation characteristics such as velocity and direction of propagation within each segment. The mean duration of phase 3 activity was not affected in the first segment but increased significantly in the distal three segments (p less than 0.05). The propagation of migrating myoelectric complexes across the sites of transection and reanastomosis started recovering 45-60 days after surgery and recovered fully by 98-108 days. The study findings show that enteric mechanisms control the initiation of migrating myoelectric complexes. Each small segment of the small intestine is capable of initiating migrating myoelectric complexes of its own and behaves as a relaxation oscillator. In the intact small intestine, regional migrating myoelectric complex oscillators are coupled by the intrinsic neurons so that the proximal oscillators drive the distal oscillators. Recovery of migrating myoelectric complex propagation across sites of transection and reanastomosis suggest that intrinsic nerves regenerate after transection.

Action Potentials↗

PubMed1994

Migration of acute lymphoblastic leukemia cells into human bone marrow stroma.

Most cases of acute lymphoblastic leukemia (ALL) arise from malignant transformation of B-cell precursors in the bone marrow. Recent studies have shown that normal and leukemic B-cell precursors bind to bone marrow stromal cells through the beta-1 integrins VLA-4 and VLA-5, thereby exposing early lymphoid cells to regulatory cytokines. It has been recently reported that the pre-B cell line NALM-6 is capable of migrating under layers of murine stromal cells in vitro (Miyake et al. J Cell Biol 1992;119:653-662). We have further analyzed leukemic cell motility using human bone marrow fibroblasts (BMF) as a stromal layer. The precursor-B ALL cell line NALM-6 rapidly adhered to BMF, and underwent migration or tunneling into BMF layers within 5 h, as demonstrated by light and electron microscopy, and confirmed by a chromium-labeling assay. Migration was also observed with the precursor-B ALL lines Reh and KM-3, with a T leukemia line RPMI-8402, the monocytic line U937, and the mature B line Daudi. In contrast, mature B (Raji), myeloid (K562, HL-60), and T lines (CCRF-CEM, MOLT-4) did not migrate. When cases of leukemia were analyzed, BMF migration was largely confined to precursor-B ALL, occurring in eight of 13 cases tested. Of other types of leukemia, migration was observed in one of four cases of T-ALL, but no evidence was seen in six acute myeloid leukemias and two patients with chronic lymphocytic leukemia. Only minimal migration into BMF was observed with purified sorted CD10+ CD19+ early B cells from normal adult marrow, while normal mature B lymphocytes from peripheral blood did not migrate. ALL migration was inhibited by monoclonal antibodies to the beta sub-unit of the VLA integrin family, and by a combination of antibodies to VLA-4 and VLA-5. Partial inhibition was also observed when leukemic cells were incubated with antibodies to VLA-4, VLA-5, or VLA-6 alone. In contrast, treatment of stromal cells with antibodies to vascular cell adhesion molecule or fibronectin (ligands of VLA-4 and VLA-5) did not prevent leukemic cell migration. These results indicate that ALL cells are highly motile and capable of rapid migration within marrow stroma, an effect largely mediated by VLA-4 and VLA-5. In the case of precursor-B ALL, this process may reflect a homing mechanism to areas of selective growth advantage within the bone marrow microenvironment.

Antigens, CD↗

PubMedDate not supplied

[The social organization, behavior and ecological parameters of a migrating population of Siberian roe deer (Capreolus pygargus Pall.)].

Data obtained in 1988-1994 during a long-term study of the ecology and behavior of a seasonally migrating Siberian roe population in Amur Province are reviewed. Aerial surveillance of 24 roe marked with transmitters was used for tracing their migration routes under normal conditions and in the homing experiment. It was found that the routes of roe migrations can be as long as 200 km. These routes, as well as summer and winter territories and the sites where roe cross the rivers, remain unchanged year after year. In spring, roe migrate back along the same route as in autumn. In autumn, the average rate of migration is 6.1 km per day (the maximum rate is 26 km per day), and in summer it is 3.8 km per day. The urge to migrate is apparently innate. The roe memorize the route followed once and are capable of orienting themselves on expanses of land. The first frosts provide a stimulus for autumn migrations. Most roe start to migrate 30-45 days before the formation of snow cover, when forage is still abundant. This fact contradicts traditional views on roe migrations, which fall into the following scheme: thick snow cover; the absence of forage; migrations. A new hypothesis concerning the evolution of roe migrations is proposed. The social, sex, and age structures of the population are analyzed.

Animals↗

PubMed1994

Human keratinocyte migration on type IV collagen. Roles of heparin-binding site and alpha 2 beta 1 integrin.

BACKGROUND: The migration of human keratinocytes is an early and important event in the re-epithelialization of cutaneous wounds. Type IV collagen, a ubiquitous basement membrane component, promotes keratinocyte migration. EXPERIMENTAL DESIGN: In this study, we sought to identify specific sites within the type IV collagen molecule that induce keratinocyte locomotion and to characterize the cell surface receptors involved. We first examined purified fragments of the type IV collagen molecule as substrates for keratinocytes in a phagokinetic migration assay. We then tested several synthetic peptides derived from the triple-helical region of type IV collagen, as well as antibodies against specific integrin subunits, for their ability to either support or inhibit keratinocyte migration on matrices of both type IV collagen and relevant peptide derivatives. RESULTS: Keratinocytes migrated on the triple-helical fragment to the same extent as they did on the native type IV collagen. The amino-terminal 7S and the carboxy-terminal NC1 regions of type IV collagen failed to support keratinocyte migration. In addition, Hep III peptide was active both in inhibiting keratinocyte migration on type IV collagen and in serving as a substrate matrix for migration. Peptide containing the amino acid sequence RGD did not influence cell migration on type IV collagen. A specific monoclonal antibody against the alpha 2 beta 1 integrin receptor significantly inhibited keratinocyte migration on matrices of both type IV collagen and Hep III peptide. CONCLUSIONS: Keratinocyte migration on type IV collagen involves the interaction of the alpha 2 beta 1 receptor with the Hep III region of the type IV collagen molecule.

Binding Sites↗

PubMed1994

Effect of in vitro and in vivo migration of bovine neutrophils on binding and expression of Fc receptors for IgG2 and IgM.

Binding of endogenous and exogenous homologous IgG2 and IgM to bovine neutrophils before and after in vitro migration through micropore filters, and in vivo migration through mammary tissues after intramammary injection of endotoxin was evaluated by use of flow cytometry. Immunoglobulin binding to neutrophils at 4 and 37 C was also evaluated. Before and after in vitro migration, neutrophils with endogenously bound IgG2 and IgM averaged 1 and 2% and 23 and 7%, respectively. Before and after in vivo migration, IgG2 and IgM binding averaged 1 and 7% and 26 and 15%, respectively. Before and after in vitro migration, binding of purified IgG2 and IgM averaged 75 and 67% and 8 and 24%, respectively. Before and after in vivo migration, percentage of neutrophils binding purified IgG2 and IgM averaged 92 and 98% and 54 and 70%, respectively. When serum was used as a source of exogenous immunoglobulins, binding of total IgG after in vitro migration increased from 5% to 28% and of IgM from 4% to 20%. After in vivo migration, binding increased from 21% to 47% and from 24% to 56%, respectively. Exogenous binding of IgG2 at 4 and 37 C averaged 75 and 84%, and binding of IgM averaged 8% at either temperature. Endogenous IgG2 was unaffected by temperature, however, binding of IgM decreased from 23% at 4 C to 2% at 37 C. These data indicate that endogenous binding was higher for IgM before migration than after migration, in vitro and in vivo. Furthermore, migration in vivo through cellular matrices induced receptor upregulation for IgG and IgM.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Quantitation and kinetics of blood monocyte migration to acute inflammatory reactions, and IL-1 alpha, tumor necrosis factor-alpha, and IFN-gamma.

Monocytes migrate from the blood into acute inflammatory reactions, where they differentiate into macrophages, and after 12 to 24 h become the predominant histologic feature of the inflammatory infiltrate. The quantitation of monocyte migration into these reactions has been difficult. This report employs a novel combination of techniques to isolate highly purified monocytes from the blood of rats, and shows that these cells have a normal t1/2 of 26 h and migrate efficiently after i.v. injection into cutaneous acute inflammatory sites. Monocytes labeled with 51Cr accumulated in delayed-type hypersensitivity reactions, and sites injected with killed Escherichia coli, LPS, poly-inosine: cytosine, zymosan-activated serum (ZAS), a source of C5adesArg, and the cytokines IL-1 alpha, TNF-alpha, and IFN-gamma. Both radiolabeled monocytes and neutrophils migrated rapidly to E. coli, LPS, ZAS, IL-1 alpha, and TNF-alpha with a large increase in cell accumulation by 2 h. Neutrophil migration declined rapidly to undetectable levels by 3 to 4 h to all five stimuli, and monocyte migration to ZAS and IL-1 alpha also declined by this time. In contrast, E. coli, LPS, and TNF-alpha caused a sustained migration of monocytes for 5 to 6 h, long after neutrophils had stopped accumulating. Intradermal IFN-gamma did not recruit neutrophils but stimulated a prolonged monocyte migration from 1 to 6 h. Combinations of LPS, TNF-alpha, and IFN-gamma synergistically enhanced the late (> 5 h) but not the early phase of monocyte recruitment. In conclusion, purified monocytes isolated from rat blood can be used to quantify monocyte migration in vivo, and these cells migrate rapidly to cutaneous inflammation and in response to chemotactic factors, IL-1 alpha, TNF-alpha, and IFN-gamma, with initial kinetics similar to those of neutrophils. However, monocyte-selective mechanisms are induced by IFN-gamma and also appear to be involved in prolonged monocyte migration to TNF-alpha, LPS, and E. coli.

Acute Disease↗

PubMed1993

Fibroblast migration in fibrin gel matrices.

In healing wounds and many solid tumors, locally increased microvascular permeability results in extravasation of fibrinogen and its extravascular coagulation to form a fibrin gel, with concomitant covalent cross-linking of fibrin by factor XIIIa. Subsequently, inflammatory cells, fibroblasts, and endothelial cells migrate into the gel and organize it into granulation tissue and later into mature collagenous connective tissue. To gain insight into some of the cell migration events associated with these processes, we developed a quantitative in vitro assay that permits the study of fibroblast migration in fibrin gels. Early passage human or rat fibroblasts were allowed to attach to tissue culture dishes and then were overlaid with a thin layer of fibrinogen that was clotted with thrombin. Fibroblasts began to migrate upwards into the fibrin within 24 hours and their numbers and the distance migrated were quantified over several days. The extent of fibroblast migration was affected importantly by the nature of the fibrin clot. Fibroblasts migrated optimally into gels prepared from fibrinogen at concentrations of -3 mg/ml; ie, near normal plasma fibrinogen levels. Migration was greatly enhanced by extensive cross-linking of the fibrin alpha-chains by factor XIIIa, as occurs when clotting takes place in vivo. When fibrinogen was clotted in Dulbecco's modified Eagle's medium, gamma-chains were cross-linked, but alpha-chain cross-linking was strikingly inhibited, and fibroblasts migrated poorly. Gels prepared from factor XIII-depleted fibrinogen exhibited neither alpha-nor gamma-chain cross-linking and did not support fibroblast migration. Further purification of fibrinogen by anion exchange high pressure liquid chromatography depleted fibrinogen of fibronectin, plasminogen, and other impurities; this purified fibrinogen clotted to form fibrin gels that supported reproducible fibroblast migration.

Animals↗

PubMed1996

Migration of brain tumor cells on extracellular matrix proteins in vitro correlates with tumor type and grade and involves alphaV and beta1 integrins.

An important contributor to the malignancy of brain tumors is their ability to infiltrate the brain. Extracellular matrix molecules and cell adhesion molecules on cell surfaces play key roles in cell migration. In the present study, we used reaggregates of dissociated cells from freshly excised human brain tumors to analyze the migration of cells from human brain tumors of different types and grades on many different adhesion proteins adsorbed to glass substrates. Proteins were chosen based on their presence in normal or neoplastic nervous tissue, and included the extra-cellular matrix molecules fibronectin, collagens, fibrinogen, laminin, tenascin-C, thrombospondin, and the neuron-glia cell adhesion molecule, Ng-CAM. Cells from astrocytomas (n = 24) migrated on a variety of substrates, in contrast to cells from primitive neuroectodermal tumors cells (n=6), which only migrated well on laminin, fibronectin, or type IV collagen but not on the other substrates. Typically, migrating cells from astrocytomas of all grades had long, slender processes, were usually bipolar, and their cell bodies did not spread well on any substrate. Although there was variability in the migration of cells from astrocytomas of the same grade, cells from high-grade astrocytomas tended to migrate more extensively (42.3 +/- 4.7 micrometers/16 h: n = 16) than cells from lower grade astrocytomas (28.9 +/- 3.9 micrometers/16 h; P = 0.07; n = 8); the most striking differences were observed for collagen substrates, on which cells from lower grade astrocytomas migrated at very low levels (7.6 +/- 2 .6 micrometers/16 h) and cells from high-grade astrocytomas at higher levels (24.4 +/- 5.2 micrometers;P = 0.01). In contrast to primary cells from glioblastomas (n = 13), glioblastoma cell lines (n = 10) consistently spread on various substrates and migrated at high levels (69.5 +/- 7.6 versus 46.4 +/-5.7 micrometers/16 h; P = 0.03), in particular, on collagens (108.4 +/- 20.2 versus 28.0 +/- 6.1 micrometers/16 h; P= 0.001). Specific monoclonal antibodies to alphaV and beta1 integrin monomers completely inhibited the migration of astrocytoma cells on most substrates, suggesting that alphaV and beta1 integrins play a crucial role in brain tumor infiltration. These studies also suggest that although a large number of extracellular matrix molecules may promote tumor cell migration, disrupting the function of only a few tumor cell receptors may be critical for tumor infiltration in the brain.

Antibodies↗

PubMed1996

Impaired migration in vitro of neutrophils from patients with paroxysmal nocturnal haemoglobinuria.

Migration of neutrophils in patients with paroxysmal nocturnal haemoglobinuria (PNH) was studied using two different complement-free in vitro model systems, subagarose and transendothelial migration. In the subagarose migration assay the mean migration distance of PNH neutrophils was slightly, but significantly, reduced to 1236 microns (range 753-1586, n = 6) compared to a normal mean of 1476 microns (range 1076-1768, n = 6, P = 0.016). By immunocytochemical staining for the urokinase type plasminogen activator receptor (uPAR) which is a glycosyl-phosphatidyl-inositol (GPI) anchored protein expressed by normal, but not by PNH-affected, neutrophils, it was shown that the uPAR-positive subpopulation of normal neutrophils predominated among the faster migrating cells (60-80% normal cells at the front of migration) while uPAR-negative (i.e. PNH-affected neutrophils) were more numerous close to the application well (5-30% normal cells). When migration of neutrophils was tested across a monolayer of human umbilical vein endothelial cells (HUVEC) cultured on polycarbonate filters, there was a 3-4-fold impairment of the migration of the PNH-affected neutrophils both in the absence of stimulation and after stimulation with fMLP (P < 0.001 in both cases). After IL-1 stimulation of the endothelium the impairment was even more pronounced (8-fold difference, P < 0.001). When the endothelial cells were grown on collagen-coated filters the impairment of the migration of PNH neutrophils was less pronounced, but still significant after stimulation with fMLP and IL-1 (2-fold, P < 0.05 in both cases). These results demonstrate that there is a complement-independent impairment of migration of neutrophils from patients with PNH which may be related to their failure to express GPI-linked proteins involved in cell migration and/or adhesion such as the uPA receptor and the CD66b antigen.

Cell Movement↗

PubMedDate not supplied

[Migration and health].

In the last decades of this century we are witnesses of frequent crises in different parts of the world produced by internal disturbance and wars. These crises, together with natural disasters, poverty and hunger, follow the history of mankind often forcing huge population groups to leave their homes. The harmful health consequences are among negative effects of migrations. While stable populations have well-tried routines for maintaining health, migrations mean abandoning such support systems. The increased exposure to harmful factors contributes more to the bad health condition of the migrant population. Setting of newcomers and local people together in the same homes, reduction in food and heating resources, drug shortage as well as importation of new infectious agents, may also endanger health of the native population. These observations have also been confirmed by Yugoslav experience. Depending on the fact whether a migration is elemental or organized i.e. dependent on its place in the large scale between these two extreme endpoints, the size of risk is also dependent on the consequences and degree of their difficulty. Mass health disturbances occur during migrations of the population from war regions, migrations from areas of natural disasters, mass pilgrimage, migrations of seasonal workers and migrations of armies during wars. However, even in these difficult times and conditions, a good organization can contribute to the mitigation of harmful consequences caused by these migrations. For instance, in 1942 there was an epidemic of typhus fever in Bosnia when many refugees crossed the Drina river on the way to Serbia escaping from Ustasha terrorism. At the Serbian side there were checkpoints where the refugees could taka a bath and where their laundry and clothing were depediculated with dry air, and after a two-week quarantine they could continue to Serbian provinces without making new foci of typhus fever. The most vulnerable and numerous group of refugees is usually composed of women, children and old persons. One of the largest migrations took place over the period from 1991 to 1995, when about 1,500,000 people left the war areas of the former Yugoslavia, Bosnia-Herzegovina and Croatia. Of that number, about 700.000 refugees came to Yugoslavia. In August 1995 during an unprecedented exile from the Kninska krajina region (Croatia) over 200,000 people left their homes. During the arrival of refugees and expelled persons health teams offered first aid to these unlucky persons at reception points: drinking water, food, emergency care and indispensable clothing. The next step in their task was to move refugees into families i.e. into collective camps and centres. As in similar situations, this migration had also its negative effects on health of the refugees. At this time, however, the situation was aggravated by international economic sanctions imposed to Yugoslavia although Yugoslavia has accepted and received more refugees than all European countries together. In 1992 a special refugees Law was promulgated in Yugoslavia. In this Law, among other things, it was stated that "the organized reception, temporary lodging, nutrition, appropriate health care, material and other sort of help" will be secured to refugees. The increased infant mortality rate in Yugoslavia may be ascribed to migrations. After several years of decrease it was in constant rise over the period from 1991 to 1995 (Table 1). Disturbed mental balance, loosing of ethic norms, feeling of hopelessness and despair, and underestimation of the risk of infections among refugees, contributed to the rise of promiscuity and increase in sexually transmitted diseases. Thus, the number of registered cases of symphills in the period 1991-1995 was six times greater than in previous years. The number of gonorrhea cases was twice greater in this period than before that time. At the same time, it should be emphasized that the number of recorded cases was smaller than it w

Aged↗

PubMed1997

Origin and route of tangentially migrating neurons in the developing neocortical intermediate zone.

Neuroblasts produced in the ventricular zone of the neocortex migrate radially and form the cortical plate, settling in an inside-out order. It is also well known that the tangential cell migration is not negligible in the embryonic neocortex. To have a better understanding of the tangential cell migration in the cortex, we disturbed the migration by making a cut in the neocortex, and we labeled the migrating cells with 1,1'-dioctodecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI) in vivo and in vitro. We also determined the birth dates of the cells. Disturbance of tangential cell migration caused an accumulation and disappearance of microtubule-associated protein 2 immunoreactive (MAP2-IR) cells on the ventral and dorsal side of the cut, respectively, which indicated that most of the MAP2-IR cells in the intermediate zone (IZ) were migrating toward the dorsal cortex. The DiI injection study in vivo confirmed the tendency of the direction of cell migration and suggested the origin of the cells to be in the lateral ganglionic eminence (LGE). DiI injection into the LGE in vitro confirmed that the LGE cells cross the corticostriatal boundary and enter the IZ of the neocortex. The migrating cells acquired multipolar shape in the IZ of the dorsal cortex and seemed to reside there. A 5-bromo-deoxyuridine incorporation study revealed that the migrating MAP2-IR cells in the IZ were early-generated neurons. We concluded that the majority of tangentially migrating cells were generated in the LGE and identified as a distinct population that was assumed not to have joined the cortical plate.

Animals↗