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At least 487 records · Page 27Linked to original sources
PubMed2002

The urokinase receptor mediates basic fibroblast growth factor-dependent smooth muscle cell migration through baboon aortic explants.

The urokinase receptor is required for vascular smooth muscle cell migration in vitro, but may not be needed in vivo since smooth muscle cell migration and intimal hyperplasia after arterial injury in mice are not affected by urokinase receptor gene deletion. We have used baboon aortic explants as a bridge between cell culture and in vivo experiments to determine if the urokinase receptor is required for smooth muscle cell proliferation and smooth muscle cell migration in primate vessels. Levels of urokinase receptor in explants increased with time after explantation, while blockade of urokinase receptor with an antibody decreased smooth muscle cell proliferation and smooth muscle cell migration from the explants. A blocking antibody to basic fibroblast growth decreased levels of urokinase and urokinase receptor in explants, and it decreased smooth muscle cell migration and mitogenesis. These results suggest that the factor urokinase receptor plays a positive role in smooth muscle cell migration and proliferation in injured primate arterial tissue, in part mediating the pro-migratory and proliferative effects of basic fibroblast growth factor released by damaged smooth muscle cells.

Animals↗
PubMed1998

MR features of developing periventricular white matter in preterm infants: evidence of glial cell migration.

PURPOSE: MR imaging of the brain is increasingly used in the investigation of the newborn, but little information is available on the normal appearance of the developing brain. We scanned a series of newborn infants in an attempt to define the normal appearance of developing periventricular white matter and to assess how pathologic conditions may modify this appearance. METHODS: Sixty-eight newborn infants, median postmenstrual age (PMA) 34 weeks (range, 24 to 42 weeks), were subdivided into two groups: group A (n = 33), which included those with normal clinical and sonographic examinations, and group B (n = 35), which contained those with evidence of neuroabnormality detected prior to the MR study, either clinically or by cerebral sonography. Images were acquired in two planes on a 1.5-T imager using turbo spin-echo pulse sequences. RESULTS: Symmetric periventricular bands of reduced signal intensity were noted in the frontal periventricular white matter on T2-weighted images in 98% of group A infants and in 97% of group B infants. The number of bands was inversely related to PMA. The reduction in number of bands with increasing PMA was delayed in group B infants. CONCLUSION: The uniform appearance of periventricular bands in a population of healthy infants and their relationship to the infants' maturity is consistent with the results of previous histologic studies. These studies demonstrate the presence of migrating glial cells within the periventricular white matter of infants beyond 20 weeks' gestation, when neuronal migration to the cortex is complete. We postulate that the bands seen on T2-weighted images represent groups of migrating glial cells, providing a further marker of cerebral maturation.

Brain↗
PubMed1986

Effects of puromycin, cycloheximide and noradrenaline on cell migration within the crypts and on the villi of the small intestine. A model to explain cell movement in both regions.

The normal process of cell migration, occurring as part of the replacement scheme within the small intestinal epithelium, was investigated extensively. The effects of puromycin, cycloheximide and noradrenaline on the movement of tritiated thymidine [( 3H]TdR) prelabelled crypt or villus cells have been studied. These studies have led to the formulation of a model for the mechanism of cell migration, postulating that the crypts and villi behave as separate units, with regard to cell migration, in addition to their distinct structural and functional properties. It is proposed that crypt cell migration is an active process requiring protein synthesis and protein glycosylation, whilst movement of villus epithelial cells is passive, depending on the continued contraction of smooth muscle cells in the lamina propria.

Animals↗
PubMed2003

Kallikrein gene transfer protects against ischemic stroke by promoting glial cell migration and inhibiting apoptosis.

Kallikrein/kinin has been shown to protect against ischemia/reperfusion-induced myocardial infarction and apoptosis. In the present study, we examined the potential neuroprotective action of kallikrein gene transfer in cerebral ischemia. Adult, male Sprague-Dawley rats were subjected to a 1-hour occlusion of the middle cerebral artery followed by intracerebroventricular injection of adenovirus harboring either the human tissue kallikrein gene or the luciferase gene. Kallikrein gene transfer significantly reduced ischemia-induced locomotor deficit scores and cerebral infarction after cerebral ischemia injury. Expression of recombinant human tissue kallikrein was identified and localized in monocytes/macrophages of rat ischemic brain by double immunostaining. Morphological analyses showed that kallikrein gene transfer enhanced the survival and migration of glial cells into the ischemic penumbra and core, as identified by immunostaining with glial fibrillary acidic protein. Cerebral ischemia markedly increased apoptotic cells, and kallikrein gene delivery reduced apoptosis to near-normal levels as seen in sham control rats. In primary cultured glial cells, kinin stimulated cell migration but inhibited hypoxia/reoxygenation-induced apoptosis in a dose-dependent manner. The effects of kinin on both migration and apoptosis were abolished by icatibant, a bradykinin B2 receptor antagonist. Enhanced cell survival after kallikrein gene transfer occurred in conjunction with markedly increased cerebral nitric oxide levels and phospho-Akt and Bcl-2 levels but reduced caspase-3 activation, NAD(P)H oxidase activity, and superoxide production. These results indicate that kallikrein gene transfer provides neuroprotection against cerebral ischemia injury by enhancing glial cell survival and migration and inhibiting apoptosis through suppression of oxidative stress and activation of the Akt-Bcl-2 signaling pathway.

Adenoviridae↗
PubMed2006

PI3K and RAC signalling in leukocyte and cancer cell migration.

Leukocytes and amoeboid-stage cancer cells migrate in a similar manner. Key signalling molecules regulating leukocyte and cancer cell migration are phosphoinositide 3-kinase (PI3K) and the Rho family of small GTPases. While PI3K activity defines the leading edge of the cell, Rho family GTPases regulate the cytoskeletal remodelling during polarisation and migration. We review here briefly the roles of PI3K, of the Rho-family GTPase Rac, and of the guanine-nucleotide exchange factors that activate Rac, in leukocyte and cancer cell migration.

Actins↗
PubMed1981

The effect of human intraocular fluid on vascular endothelial cell migration.

Several recent studies have demonstrated that vascular endothelial cell migration is an essential element of new blood vessel formation. We have recently developed an in vitro assay to study the effect of various substances on vascular endothelial cell migration. We now report the use of this assay to study the effect of human intraocular fluid on endothelial cell migration. We have found a good correlation between the presence of progressive retinal neovascularization in an eye and the ability of vitreous cavity fluid from that eye (obtained at the time of vitrectomy) to stimulate vascular endothelial cell migration in vitro.

Blood Vessels↗
PubMed2006

Syndecan-4 clustering induces cell migration in a PDZ-dependent manner.

Cell migration is a dynamic process involving formation of a leading edge in the direction of migration and adhesion points from which tension is generated to move the cell body forward. At the same time, disassembly of adhesion points occurs at the back of the cell, a region known as the trailing edge. Syndecan-4 (S4) is a transmembrane proteoglycan thought to be involved in the formation of focal adhesions. Recent studies have shown that its cytoplasmic domain can engage in signal transduction, making S4 a bona fide receptor. Here, we show that ligand clustering of cell surface S4 on endothelial cells initiates a signaling cascade that results in activation of Rac1, induction of cell polarization, and stimulation of cell migration that depends on S4 interaction with its PDZ-binding partner. Expression of an S4 mutant lacking its PDZ-binding region (S4-PDZ(-)) leads to decreased cell motility and a failure to form a trailing edge. On clustering S4, but not S4-PDZ(-), targets activated Rac1 to the leading edge of live cells. Cells lacking synectin, a PDZ domain containing protein that interacts with S4, fail to migrate in response to S4 clustering. Both S4-PDZ(-)-expressing and synectin(-/-) endothelial cells exhibit elevated basal levels of Rac1. Thus, our data suggest that S4 promotes endothelial cell migration in response to ligand binding by activating Rac1 and localizing it to the leading edge, and that these processes are dependent on its PDZ-binding domain interaction with synectin.

Adaptor Proteins, Signal Transducing↗
PubMed1976

Substrate dependence of cell migration from explanted neural tubes in vitro.

Embryonic chick neural tubes containing neural crest cells were cultured in vitro on tissue culture plastic and collagen. Two parameters, the time of onset of cell migration from the neural tube and the rate of movement of the cell front away from the neural tube explant, were determined. On collagen, cell migration consistently began after four to six h in vitro, about five h prior to the onset of cell migration on tissue culture plastic. The identity of the migrating cells as neural crest cells is established by their eventual differentiation into melanocytes. Ablation experiments reveal that collagen also causes the early onset of migration of cells not of neural crest origin. These results provide in vitro support for the idea that extracellular materials may alter cell migratory behaviour in morphogenesis.

Animals↗
PubMed2004

Rho mediates the shear-enhancement of endothelial cell migration and traction force generation.

The migration of vascular endothelial cells in vivo occurs in a fluid dynamic environment due to blood flow, but the role of hemodynamic forces in cell migration is not yet completely understood. Here we investigated the effect of shear stress, the frictional drag of blood flowing over the cell surface, on the migration speed of individual endothelial cells on fibronectin-coated surfaces, as well as the biochemical and biophysical bases underlying this shear effect. Under static conditions, cell migration speed had a bell-shaped relationship with fibronectin concentration. Shear stress significantly increased the migration speed at all fibronectin concentrations tested and shifted the bell-shaped curve upwards. Shear stress also induced the activation of Rho GTPase and increased the traction force exerted by endothelial cells on the underlying substrate, both at the leading edge and the rear, suggesting that shear stress enhances both the frontal forward-pulling force and tail retraction. The inhibition of a Rho-associated kinase, p160ROCK, decreased the traction force and migration speed under both static and shear conditions and eliminated the shear-enhancement of migration speed. Our results indicate that shear stress enhances the migration speed of endothelial cells by modulating the biophysical force of tractions through the biochemical pathway of Rho-p160ROCK.

Animals↗
PubMed1998

The role of endothelium in the regulation of hematopoietic stem cell migration.

Mobilization of hematopoietic progenitor cells appears to be a multifactorial process which is at least partially regulated at the level of bone marrow microvascular endothelium (BMEC). In order to study the regulation of progenitor cell migration by endothelium in vitro, methods have been developed to isolate BMEC from bone marrow aspirates. In addition, immortalized BMEC cell lines have been generated. Using an in vitro model of migration across bone marrow endothelium, we demonstrate that only a small number of more mature, committed progenitors migrate spontaneously. In this model, adhesion molecules of the beta2-integrin family and the corresponding endothelial ligands are involved. The low spontaneous migratory capacity suggests that, in addition to adhesion molecules which mediate direct cellular contacts, paracrine cytokines and chemokines may play a role in progenitor migration across endothelium. Growth-factor-stimulated hematopoietic cells can produce cytokines which act on endothelial cells (e.g., vascular endothelial growth factor, VEGF), modifying their motility, growth, permeability, and fenestration. Therefore, VEGF might be involved in the mobilization and homing of hematopoietic progenitor cells. Furthermore, transendothelial migration of progenitors in vitro is substantially enhanced by the chemokine stromal-cell-derived factor-1 (SDF-1), which is produced by bone marrow stromal cells. More primitive progenitors, which do not migrate spontaneously, also respond to this chemokine. We conclude that transendothelial progenitor cell migration is regulated by adhesion molecules, paracrine cytokines, and chemokines. Mobilizing hematopoietic growth factors stimulate proliferation of hematopoietic cells, which may indirectly result in changes of the local cytokine and chemokine milieu, adhesion molecule expression, and eventually the mobilization of hematopoietic progenitor cells.

Animals↗
PubMed1986

Ultrastructural appearances of subcultured aortic smooth muscle cells migrating into Millipore filters.

The ultrastructures of vascular smooth muscle cells migrating in Millipore filters were examined using a modified Boyden chamber. The cells (seventh and eighth subculture) were obtained from explants of rat aorta. Very small numbers of bipolar-shaped cells migrated deeply into the filter toward a platelet suspension added to the lower compartment. The migrating cells were richer in intermediate filaments and microtubules than the cells on the filter. The cytoskeleton was oriented along the elongated cell body, and the cortical microfilamentous mat was disorganized along the entire cell periphery. These data are discussed.

Animals↗
PubMed2005

Adult-fetal fibroblast interactions: effects on cell migration and implications for cell transplantation.

Wound healing is a complex process involving close cooperation between multiple cell types. During wound healing, fibroblasts are primarily responsible for synthesis of the replacement extracellular matrix. Fibroblast therapy is under investigation in this and other laboratories for its potential use to modulate the final outcome of the wound-healing process. This study addresses the potential interactions between transplanted and host fibroblasts, using a two-dimensional mixed culture model. Our results show that fibroblasts of two different phenotypes, fetal and adult, exhibit different speeds of in vitro migration. These migration speeds are conserved in mixed cocultures, suggesting that the migratory response is an intrinsic property of the fibroblast rather than a response to juxtacrine or paracrine signals. These results have relevance for cell-based therapies in that they demonstrate that donor fibroblasts of a different phenotype may at least partially retain that phenotype in the host environment and in the presence of endogenous fibroblasts.

Animals↗
PubMed1996

Modulation of cell migration by integrin-mediated cytoskeletal linkages and ligand-binding affinity.

Integrin cell surface adhesion receptors play a central role in mediating cell migration. We have developed a model system consisting of CHO cells ectopically expressing the alpha IIb beta 3 integrin to study integrin affinity and cytoskeletal interactions during cell migration. The alpha IIb beta 3 integrins are suited for study of integrin receptors during cell migration because they are well characterized with respect to ligand binding, cytoskeletal interactions, and signal transduction, and mutants with altered receptor function are available. The alpha IIb beta 3 receptor specifically mediates migration of alpha IIb beta 3-transfected CHO cells. The migration of transfected CHO cells was studied on a fibrinogen substrate both by time lapse videomicroscopy and by random and haptotactic transwell assays. Haptotactic and random transwell assays measured distinct aspects of migration, with the random transwell assay correlating most closely with time lapse videomicroscopy. Mutations in the cytoplasmic domains that increase ligand affinity or activation of the alpha IIb beta 3 receptor into a high affinity state by the LIBS6 antibody decreased the migration rate. Likewise, mutations that increase cytoskeletal organization without affecting affinity also decreased the migration rate. In contrast, truncation of the beta chain, which alters cytoskeletal associations as assayed by absence of focal adhesions, decreased haptotactic migration while increasing random migration. These effects on the migration rate were partially compensated for by altering substrate concentration, demonstrating optimum substrate concentrations that supported maximal migration. For example, cells expressing integrins locked in the high affinity state showed maximal migration at lower substrate concentrations than cells expressing low affinity receptor. Together, these results implicate the strength of adhesion between cell and substrate, as modulated by receptor affinity, organization of adhesive complexes, and substrate concentration, as important regulators of cell migration rate. Further, we demonstrate a dominant effect of high affinity integrin in inhibiting migration regardless of the organization of adhesive complexes. These observations have potential implications for tumor metastasis and its therapy.

Amino Acid Sequence↗
PubMed2006

New concepts regarding focal adhesion kinase promotion of cell migration and proliferation.

Focal adhesion kinase (FAK) is a non-receptor cytoplasmic tyrosine kinase that plays a key role in the regulation of proliferation and migration of normal and tumor cells. FAK associates with integrin receptors and recruits other molecules to the site of this interaction thus forming a signaling complex that transmits signals from the extracellular matrix to the cell cytoskeleton. Crk-associated substrate (CAS) family members appear to play a pivotal role in FAK regulation of cell migration. Cellular Src bound to FAK phosphorylates CAS proteins leading to the recruitment of a Crk family adaptor molecule and activation of a small GTPase and c-Jun N-terminal kinase (JNK) promoting membrane protrusion and cell migration. The relocalization of CAS and signaling through specific CAS family members appears to determine the outcome of this pathway. FAK also plays an important role in regulating cell cycle progression through transcriptional control of the cyclin D1 promoter by the Ets B and Kruppel-like factor 8 (KLF8) transcription factors. FAK regulation of cell cycle progression in tumor cells requires Erk activity, cyclin D1 transcription, and the cyclin-dependent kinase (cdk) inhibitor p27Kip1. The ability of FAK to integrate integrin and growth factor signals resulting in synergistic promotion of cell migration and proliferation, and its potential regulation by nuclear factor kappa B (NFkappaB) and p53 and a ubiquitously expressed inhibitory protein, suggest that it is remarkable in its capacity to integrate multiple extracellular and intracellular stimuli.

Animals↗
PubMed2005

Galpha12/13 is essential for directed cell migration and localized Rho-Dia1 function.

Scratch-wound assays are frequently used to study directed cell migration, a process critical for embryogenesis, invasion, and tissue repair. The function and identity of trimeric G-proteins in cell behavior during wound healing is not known. Here we show that Galpha12/13, but not Galphaq/11 or Galphai, is indispensable for coordinated and directed cell migration. In mouse embryonic fibroblasts endogenous Rho activity is present at the rear of migrating cells but also at the leading edge, whereas it is undetectable at the cell front of Galpha12/13-deficient mouse embryonic fibroblasts. Spatial activation of Rho at the wound edge can be stimulated by lysophosphatidic acid. Active Rho colocalizes with the diaphanous-related formin Dia1 at the cell front. Galpha12/13-deficient cells lack Dia1 localization to the wound edge and are unable to form orientated, stable microtubules during wound healing. Knock down of Dia1 reveals its requirement for microtubule stabilization as well as polarized cell migration. Thus, we identified Galpha12/13-proteins as essential components linking extracellular signals to localized Rho-Dia1 function during directed cell movement.

Affinity Labels↗
PubMed1983

Neural crest cell migration: requirements for exogenous fibronectin and high cell density.

Cells of the neural crest participate in a major class of cell migratory events during embryonic development. From indirect evidence, it has been suggested that fibronectin (FN) might be involved in these events. We have directly tested the role of FN in neural crest cell adhesion and migration using several in vitro model systems. Avian trunk neural crest cells adhered readily to purified plasma FN substrates and to extracellular matrices containing cellular FN. Their adhesion was inhibited by antibodies to a cell-binding fragment of FN. In contrast, these cells did not adhere to glass, type I collagen, or to bovine serum albumin in the absence of FN. Neural crest cell adhesion to laminin (LN) was significantly less than to FN; however, culturing of crest cells under conditions producing an epithelioid phenotype resulted in cells that could bind equally as well to LN as to FN. The migration of neural crest cells appeared to depend on both the substrate and the extent of cell interactions. Cells migrated substantially more rapidly on FN than on LN or type I collagen substrates; if provided a choice between stripes of FN and glass or LN, cells migrated preferentially on the FN. Migration was inhibited by antibodies against the cell-binding region of FN, and the inhibition could be reversed by a subsequent addition of exogenous FN. However, the migration on FN was random and displayed little persistence of direction unless cells were at high densities that permitted frequent contacts. The in vitro rate of migration of cells on FN-containing matrices was 50 microns/h, similar to their migration rates along the narrow regions of FN-containing extracellular matrix in migratory pathways in vivo. These results indicate that FN is important for neural crest cell adhesion and migration and that the high cell densities of neural crest cells in the transient, narrow migratory pathways found in the embryo are necessary for effective directional migration.

Animals↗
PubMed2006

The effect of RhoA on human umbilical vein endothelial cell migration and angiogenesis in vitro.

The mechanisms that control the morphologic organization of endothelial cells (ECs) into new blood vessels are not well understood. Recent studies revealed that the small G proteins of the Rho family are key regulators of cell migration, involving reorganization of the actin cytoskeleton, cell migration and the regulation of gene transcription. We hypothesized that RhoA GTPase, a member of the Rho family, may play an important role in EC organization during angiogenesis, the process of new vessel formation in pre-existing tissues. To test this hypothesis, we investigated the effects of RhoA on human umbilical vein endothelial (HUVE) cell migration and angiogenesis in vitro, by stably transfecting HUVE cells with sense RhoA expression plasmid through the Lipofect-2000 system. Wound assay in vitro and 3-dimensional cell culture were used to detect the migration and angiogenesis capacity of HUVE cells. The morphological changes of transfected cells were revealed under confocal and phase contrast microscopy. Our results demonstrated that the increased expression of RhoA in HUVE cells significantly enhanced the morphogenetic changes and cytoskeletal reorganization of the transfected cells, and also enhanced cell migration and angiogenic capacity in vitro, suggesting that RhoA plays an important role in the process of HUVE cell migration and angiogenesis in vitro.

Actins↗
PubMed2002

A non-peptide CCR5 antagonist inhibits collagen-induced arthritis by modulating T cell migration without affecting anti-collagen T cell responses.

The chemokine receptors CCR5 and CXCR3 have been implicated as playing a central role in directing a Th1 inflammatory response. Here, we investigated whether a synthetic CCR5 antagonist affects the process of T cell migration to sites of inflammation. Immunization of DBA/1 mice with type II collagen resulted in typical arthritis, which is associated with cellular infiltration. Treatment with a CCR5 antagonist strikingly affected the development of arthritis by reducing both incidence and severity of disease. There was no substantial difference between collagen-immunized mice with and without antagonist treatment in the induction of anti-collagen T cell responses and the capacity to produce IL-12. This endogenous IL-12 functioned to induce comparable levels of CCR5 in these two immunized groups of T cells. Whereas a massive infiltration of inflammatory cells including CCR5(+) T cells occurred in the joints of mice immunized without antagonist, cellular infiltration in the antagonist-treated group was only marginal. These results indicate that administration of a CCR5 antagonist inhibits the development of arthritis not by affecting the generation of collagen-sensitized T cells but by interfering with their migration to joint lesions.

Amides↗