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PubMed1993

Subpopulations of bone marrow fibroblasts support VLA-4-mediated migration of B-cell precursors.

Proliferation of normal human lymphoid progenitors in culture is dependent on interaction with bone marrow-derived fibroblast-like cells (BM-FB). To investigate possible heterogeneity in this lymphoid-supportive microenvironment, we studied the interaction of a human B-precursor cell line (NALM-6) with BM-FB. NALM-6 cells associate with BM-FB by either adhesion or migration underneath the fibroblast. Individual fibroblasts in the BM-FB layer showed significant variation in the number of migrating NALM-6 cells. Migration of NALM-6 cells was primarily VLA-4-dependent, although residual migration observable after blocking with anti-VLA-alpha 4 antibody was inhibited by anti-VLA-alpha 5 antibody. Migration was not inhibited by blocking either of the known VLA-4 counterreceptors (VCAM-1 or fibronectin), although slight inhibition was observed using a combination of blocking antibodies to VCAM-1 and fibronectin. In contrast, NALM-6 adhesion without migration was significantly inhibitable by anti-VCAM-1 antibody. VCAM-1 or fibronectin expression on individual BM-FB did not correlate with NALM-6 migration. These results indicate that the adhesion and migration of human B-lymphoid precursors in the bone marrow microenvironment are mechanistically separable events and suggest the possibility of novel VLA-4 ligand(s), which may be important in human lymphopoiesis. Subpopulations of cells in the bone marrow microenvironment may preferentially support important aspects of lymphoid progenitor development.

Adult↗
PubMed1994

Removal of olfactory placode prevents the development of LHRH neurons in the forebrain of the chick embryo: possible interaction between migrating LHRH neurons and highly polysialylated form of neural cell adhesion molecule (NCAM-H).

A unilateral olfactory placodectomy prevented the development of LHRH- and NCAM-H-expressing neurons as well as NCAM-H expressing olfactory nerve on the operated side, whereas the development of LHRH- and NCAM-H-expressing neurons and olfactory nerve was not disturbed. In the embryos with an incomplete olfactory placodectomy, a small number of LHRH-immunoreactive (ir) cells expressing NCAM-H were detected in the olfactory epithelial fragments and in the NCAM-H-positive olfactory nerve remants which ceased to extend their axons to the forebrain. The lack of the central projection of the olfactory nerve caused stagnation of LHRH-ir cells, no LHRH-ir cells being found in the forebrain. These results clearly suggest the importance of the structural support for the migration of LHRH-ir cells. Furthermore, the migrating LHRH-ir cells deviated from the poorly developed olfactory nerve and migrated not only to the central direction but also to the peripheral direction of the NCAM-H-positive medial nasal branch of the ophthalmic nerve of the trigeminal nerve. This suggests that the migration route of the LHRH neurons is not programmed in detail in the precursor cells of LHRH neurons in the olfactory placode. Since the migrating LHRH-ir cells were never independent of NCAM-H-positive neural elements in the operated embryos, it is suggested that not only the structural support for the migration but also the possible interaction between the migration of LHRH-ir cells and NCAM-H and/or other unknown factors may be needed for successful LHRH neuronal migration.

Animals↗
PubMed1994

Evidence that cell surface beta 1,4-galactosyltransferase spontaneously galactosylates an underlying laminin substrate during fibroblast migration.

beta 1,4-Galactosyltransferase is unusual among the glycosyltransferases in that a subpopulation exists on the cell surface in addition to its traditional biosynthetic location within the Golgi complex. On the cell surface, galactosyltransferase is expressed in spatially restricted, cell type-specific domains, where it functions as a receptor for extracellular oligosaccharide ligands during selected cellular interactions. For example, galactosyltransferase is found on the leading and trailing edges of migrating cells, where it facilitates lamellipodia formation and cell spreading by binding to specific N-linked oligosaccharides within laminin. Although the ability of galactosyltransferase to serve as a laminin receptor is well documented, it is unclear whether it functions solely in a lectin-like capacity to bind laminin glycoside ligands or uses its intrinsic catalytic activity to release itself from and modify its oligosaccharide substrate. In this study, we determined whether cell surface galactosyltransferase spontaneously galactosylates laminin matrices during cell migration using endogenous galactose donors. Cells were prelabeled with [3H]galactose, washed, and transferred in small clusters onto laminin matrices. The prelabeled cells migrated out from the cell cluster, during which time they deposited covalently bound [3H]galactose residues onto the laminin matrix. The degree of galactosylation was both laminin- and time-dependent and required actively migrating, intact cells. The radioactivity released from the 3H-galactosylated laminin by acid hydrolysis comigrated with authentic galactose standards on paper chromatography. In parallel assays, there was no radioactivity deposited on laminin matrices when cells were prelabeled with [3H]fucose or [3H]leucine. Furthermore, [3H]galactosylation was dependent upon galactosyltransferase-mediated cell migration, since prelabeled cells did not deposit [3H]galactose when migrating on fibronectin, upon which migration is integrin-dependent and galactosyltransferase-independent. These results raise the possibility that galactosyltransferase functions catalytically during cell migration, either to dissociate from its oligosaccharide ligand and/or to modify the extracellular matrix.

3T3 Cells↗
PubMed1994

Early migration and late aseptic failure of proximal femoral prostheses.

The vertical migration of four configurations of a proximal femoral prosthesis, followed for up to nine years, was measured on standard radiographs. The same implant was used without cement (group 1) and with cement (group 2). The migration of both groups was linear from six months onwards. The mean migration rate and the incidence of late aseptic loosening were both greater in group 1. Survival analysis of the two groups, however, showed no statistically significant difference. In both groups, hips later destined for revision migrated more rapidly from the initial postoperative period onwards, than did the remainder. A threshold migration of 1.2 mm/year during the first two years after implantation detected hips likely to fail with a specificity of 86% and a sensitivity of 78%. This 'migration test' was applied to the results in two further groups of patients in which a modified femoral prosthesis had been implanted without hydroxyapatite coating (group 3) and with hydroxyapatite coating (group 4). The test distinguished between the four groups and suggested that at least two fixation procedures should be abandoned. We conclude that vertical migration measured on standard radiographs in the first two years after implantation can be used to predict late aseptic loosening. New prosthetic configurations should be evaluated by migration measurements before their general release. Our observations support the view that one cause of late aseptic loosening is imperfect initial fixation.

Adult↗
PubMed1993

Basic fibroblast growth factor: its role in the control of smooth muscle cell migration.

The formation of an intimal lesion in an injured artery is the consequence of the replication and migration of smooth muscle cells. Recent studies have implicated basic fibroblast growth factor (bFGF) as an important mediator of replication in the arterial media, and platelet-derived growth factor as an important mediator of migration. However, the degree of arterial trauma produced during injury has a significant influence on the time of onset of intimal thickening, suggesting that factors released from damaged smooth muscle cells may affect migration. We have investigated the role of one of these factors, bFGF, in smooth muscle cell migration in vivo. We found that 1) deendothelialization of the rat carotid artery results in significantly more migration when it is accompanied by traumatic injury to the underlying smooth muscle; 2) the rate of migration in arteries that have been gently deendothelialized is significantly stimulated by systemic injection of bFGF; and 3) inhibition of bFGF with a blocking antibody significantly reduces the amount of migration after traumatic deendothelializing injury with a balloon catheter. These findings suggest that bFGF plays an important role in the mediation of smooth muscle cell migration after arterial injury.

Animals↗
PubMed1993

Protein kinase C transduces the signal for Langerhans' cell migration from the epidermis.

Langerhans' cells (LC) take up antigen in the epidermis and then migrate to the local lymph nodes where they present the antigen to T lymphocytes, initiating cutaneous immune responses. However the intracellular mechanisms which mediate LC migration from the epidermis are unknown. We have demonstrated that activation of protein kinase C (PKC) induces this LC migration. An analogue of diacylglycerol (DAG), the physiological activator of PKC, L-alpha-dioctanoyl glycerol (oDAG), applied topically onto the skin of mice caused a significant depletion in the density of Ia+ and J11d+ epidermal LC. oDAG decreased the density of LC in both BALB/c and C57BL mice 24 hr following application, over a dose range of 0.5-24 microM; 200 or 0.05 microM being ineffective. LC density remained depressed for up to 7 days and oDAG increased the number of fluorescein isothiocyanate (FITC) positive cells in the local lymph nodes of mice treated topically with FITC, indicating that oDAG induced LC migration from the epidermis. Additionally, LC migration from the epidermis induced by the contact sensitizer 2,4,6-trinitrochlorobenzene (TNCB) was blocked when PKC was inhibited by palmitoyl-DL-carnitine chloride (PCC) or D-Sphingosine (Sph), indicating that LC cannot migrate from the epidermis when PKC is inhibited. However, PCC did not inhibit the induction of contact sensitivity. Thus PKC transduces the signal which leads to LC migration from the epidermis, and disruptions in this secondary messenger may interfere with the induction of immune responses in the skin by disturbing LC migration from the epidermis to the local lymph nodes.

Administration, Topical↗
PubMed1993

Role of urokinase type plasminogen activator (u-PA) in corneal epithelial migration.

The role of plasminogen activator (PA) in the migration of corneal reepithelialization was studied. Rabbit corneal blocks were cultured, and both the extent of epithelial migration over the exposed corneal stroma and the activity of PA released into the culture media were measured. A significant, direct correlation between epithelial migration and PA activity in the medium was observed, even when the migration was stimulated by fibronectin or EGF, or was inhibited by cytochalasin B or cycloheximide. Zymography confirmed that the PA released into the culture medium was of the urokinase type (u-PA). Immunohistochemical studies showed that u-PA and plasmin(ogen) were present at the leading edge of the migrating epithelium. Studies of corneal cell cultures indicated that epithelial cells rather than endothelial cells or fibroblasts were the source of the u-PA. The addition of antihuman u-PA IgG or protease inhibitors retarded the migration of the corneal epithelium in a dose-dependent manner, indicating that u-PA activity is essential for the migration of the corneal epithelium. These findings suggest that the migration of corneal epithelial cells requires not only cell attachment to the extracellular matrix through the fibronectin but also degradation of the fibronectin by the release of cellular u-PA.

Animals↗
PubMed1996

Early migration predicts late aseptic failure of hip sockets.

We report a prospective, stratified study of 60 PCA-cups and 60 RM-polyethylene cups which have been followed for a median time of 90 months, with annual radiography. The radiological migration of cups was measured by the computer-assisted EBRA method. A number of threshold migration rates from 1 mm in the first year to 1 mm in five years have been assessed and related to clinically determined revision rates. A total of 28 cups showed a total migration of 1 mm or more within the first two years; 13 of these cups have required revision and been exchanged. The survival curves of cups which had previously shown early migration were considerably different from those without early migration. For cups with a migration of less than 1 mm within the first two years the mean survival at 96 months was 0.96 +/- 0.02; for migrating cups, it was 0.63 +/- 0.11 (log-rank test, p=0.0001; chi-square value=39.4). Early migration is a good predictor for late loosening of hip sockets.

Aged↗
PubMed1996

Quantification of bovine neutrophil migration across mammary epithelium in vitro.

A microassay system was developed to quantify bovine neutrophil transepithelial migration in vitro. The bovine mammary epithelial cell line (MAC-T) formed a confluent monolayer that served as a biologically meaningful barrier for neutrophil migration. Neutrophils added into the upper compartment of an inverted monolayer were driven to migrate across the epithelium from a basal-to-apical direction by the addition of zymosan activated serum (ZAS) into the lower compartment. The numbers of migrated neutrophils were determined by assaying the neutrophil azurophilic granule marker, myeloperoxidase. Results showed that ZAS stimulated neutrophil migration across the epithelium in a time-and dose-dependent manner. In the presence of 5% ZAS and 2 x 10(6) neutrophils, approximately 2.4 x 10(5) neutrophils migrated across the epithelium in 120 min. The procedures we have developed in this study provide a simple precisely controlled system to investigate the normal dynamics of bovine neutrophil transepithelial migration and a means to detect and study impaired neutrophil migration.

Animals↗
PubMed1996

Influence of native and modified lipoproteins on migration of mouse peritoneal macrophages and the effect of the antioxidants vitamin E and Probucol.

Macrophage-derived foam cells are a key component of the atherosclerotic plaque. Stimulation of the migration of foam cells back to the blood potentially offers an approach to plaque regression. However, information on the natural and synthetic factors influencing macrophage migration remains limited. The aim of the present study was to determine the effects of different lipoproteins and antioxidants on the migration of mouse peritoneal macrophages and macrophage-derived foam cells. The migration of cells was determined in vitro by using a Boyden chamber. Cellular content of cholesterol and cholesteryl esters was measured by HPLC. The native lipoproteins, VLDL, LDL, and HDL, and the chemically modified lipoproteins acetylated LDL (acLDL) and oxidized LDL (oxLDL), all acted as chemoattractants for macrophages that had not been lipid-loaded. The antioxidants vitamin E and Probucol had chemoattractive and chemokinetic effects on the migration of unloaded mouse peritoneal macrophages. Foam cells (lipid-laden macrophages) showed decreased mobility with increased cellular lipid content. However, as macrophages accumulated higher amounts of cholesterol and cholesteryl esters, the additional decrease of cell migration was relatively minor. Simultaneous incubation of macrophages with acLDL and vitamin E or Probucol increased migration. The content of cellular cholesterol and cholesteryl esters was not changed when acLDL-treated cells were exposed at the same time to vitamin E, but cholesteryl ester content was increased in the presence of Probucol. Overall, the findings indicate that the antioxidants vitamin E and Probucol have a potential anti-atherogenic action in stimulating migration of lipid-laden macrophages without major impairment of the ability of the cells to accumulate and metabolize modified LDL.

Animals↗
PubMed1997

Enhanced induction of very late antigen 4/lymphocyte function-associated antigen 1-dependent T-cell migration to tumor sites following administration of interleukin 12.

Administration of interleukin 12 (IL-12) into mice bearing CSA1M, OV-HM, Meth A, or MCH-1-A1 tumor induced complete regression of CSA1M and OV-HM tumors but induced only a slight growth inhibition of Meth A and MCH-1-A1 tumors. These effects of IL-12 were associated with high and only marginal levels of T-cell infiltration into CSA1M/OV-HM and Meth A/MCH-1-A1 tumor masses, respectively. Here, we investigated the role of IL-12 in the induction of T-cell migration. Spleen cells from untreated or IL-12-treated CSA1M-bearing mice were stained in vitro with a fluorescein chemical and transferred i.v. into IL-12-untreated CSA1M-bearing mice. Migration of donor cells was quantitated by counting the number of fluorescent cells on cryostat sections of tumor masses. Although only a slight migration was detected for spleen cells from IL-12-untreated CSA1M-bearing as well as IL-12-treated or untreated normal mice, enhanced migration was observed for cells from IL-12-treated CSA1M-bearing mice. A similar enhanced migration was observed for the OV-HM model. In contrast, such an enhancement was only marginal in the Meth A and MCH-1-A1 models. Immunohistochemical studies of tumors from IL-12-treated mice revealed that the predominant T-cell subset was CD4+ in CSA1M and CD8+ in OV-HM tumor masses. Consistent with this observation, the dominant subset of migrating T cells was found to be CD4+ in the CSA1M and CD8+ in the OV-HM models. T-cell migration was inhibited by pretreatment of recipients with either combination of anti-very late antigen 4 + anti-vascular cell adhesion molecule 1 or anti-lymphocyte function-associated antigen 1 + anti-intercellular adhesion molecule 1 monoclonal antibody. These results indicate that IL-12 can confer T cells with a capacity to migrate to tumor sites through very late antigen 4/lymphocyte function-associated antigen 1 adhesion pathways and that the in vivo acquisition of such a capacity following IL-12 treatment correlates with the induction of tumor regression.

Animals↗
PubMed1997

Specific domains of fibronectin mediate adhesion and migration of early murine erythroid progenitors.

The binding of late stage erythroid cells to fibronectin (FN) has been well characterized and is believed to be critical for the terminal stages of erythroid differentiation, but the adhesive properties of more primitive murine erythroid progenitors and the role of these interactions during earlier stages of erythropoiesis has not been determined. Using chymotryptic fragments and inhibitory probes, we have tested the ability of each of the major cell binding domains of FN; the RGDS sequence, the CS-1 sequence, and the carboxy-terminal heparin-binding domain (HBD), to promote adhesion of primitive burst-forming unit-erythroid (BFU-E), mature BFU-E, and colony-forming unit-erythroid (CFU-E). We found that only 10% to 15% of BFU-E bound to FN or to the RGDS sequence in contrast to 75% to 85% of CFU-E. Approximately 50% to 70% of BFU-E and 60% to 80% of CFU-E bound to the carboxy-terminal HBD and to the CS-1 sequence. The binding of BFU-E and CFU-E to the RGDS and CS-1 sites was blocked by beta1 integrin antibodies. These results suggest that binding to FN determinants is developmentally regulated during early erythroid differentiation. Erythroid progenitor migration within the bone marrow is thought to be important for the eventual release of reticulocytes into the circulation. A correlation between FN binding and the migratory capacity of erythroid cells has been suggested, although the ability of FN to promote migration of erythroid progenitors has not been directly measured. We measured migration of CFU-E on fragments of FN containing each cell binding region. CS-1-containing fragments, in addition to promoting adhesion of both BFU-E and CFU-E, supported the highest levels of CFU-E migration (11-fold above background). Migration was sixfold above background on intact FN and only threefold above background on RGDS-containing fragments. Fragments containing HBD alone, although they promoted adhesion of CFU-E, failed to support significant levels of migration. These results show that specific domains of FN possess distinct adhesion- and migration-promoting properties for murine erythroid progenitors. Regulation of the adhesive properties during erythroid differentiation may alter the ability of progenitors to migrate in the bone marrow and thus play an important role in normal murine erythroid differentiation.

Amino Acid Sequence↗
PubMed1997

Changes of neutrophil migration without modification of in vitro metabolism and adhesion in Behçet's disease.

OBJECTIVE: Increase of neutrophil chemotaxis in Behçet's disease (BD) has been described, but it is not clear whether there is a correlation with other variables of neutrophil function and whether these modifications correlate with disease activity. METHODS: We studied neutrophil functions in patients with BD in the acute phase in comparison with healthy control subjects and with the same patients during disease remission, with or without therapy. We investigated in vivo neutrophil migration by Senn's skin window technique and measured adhesion assay and superoxide production in circulating and migrating neutrophils after different stimuli. RESULTS: Neutrophil migration in vivo was 101.3 +/- 17.9 x 10(6) polymorphonuclear lymphocytes (PMN)/cm2/24 h in patients with BD in the acute phase and 66.1 +/- 7.8 x 10(6) PMN/cm2/24 h in controls (p < 0.001). No correlation was found between leukocyte counts and neutrophil migration. Neutrophil migration evaluated in the same patients in a phase of disease remission was 58.3 +/- 10.3 x 10(6) PMN/cm2/24 h (p < 0.001 vs acute phase, not significant vs controls). The neutrophils of the exudate were normally primed to response to the chemotactic peptide fMLP. No differences between the 2 groups were found in superoxide production, adhesion under basal conditions, or in response to different stimuli by circulating and migrating neutrophils. CONCLUSION: Abnormally high migration of neutrophils in the active phase of BD is the only consistent neutrophil dysfunction. Since this modification is reversed by therapy, the evaluation of in vivo neutrophil migration may be useful in diagnosing and monitoring disease activity. Blood neutrophils have normal responses to different stimuli, indicating they are not primed by the disease state.

Adult↗
PubMed1997

Coronary artery smooth muscle in culture: migration of heterogeneous cell populations from vessel wall.

A method for establishing primary cultures of smooth muscle cells (SMCs) from the porcine coronary artery without either microdissection and/or enzymatic dispersion was developed using selective migration of cells from coronary explants in vitro. This culture method relies on the heterogeneity of cell types and differences in their migration and adherence ability to separate SMC from contaminating fibroblasts or endothelial cells. The cell type was determined by immunohistochemical staining with monoclonal antibodies to SM alpha-actin, SM myosin, h-caldesmon and von Willebrand factor. The first wave of migration (1-7 days) consisted of a mixture of fibroblasts and SMCs. Only SMCs were present in the second wave of migration (7-14 days). Endothelial cells, which exhibited a lower capacity for migration and adherence, were restricted to the third wave of migration (14-21 days). Cells obtained from the second wave of migration exhibited the characteristic single-layered, aligned, hill-and-valley pattern of SMCs when confluent. Quiescence was attained 4-5 days after removal of serum, as established by [3H]-thymidine incorporation. Stimulation of the quiescent SMCs with 20% FBS resulted in a synchronous re-entry into the cell-cycle with S phase reached 15-18 h later. The SMCs prepared using this protocol thus exhibit the structural markers and capacity to undergo phenotypic modulation that are characteristic of SMCs in vivo. This approach to establishing primary cultures of SMCs offers the advantage of selecting for the subpopulation of cells capable of migration in response to injury or growth factor stimulation.

Animals↗
PubMed1997

Depressed Langerhans cell migration and reduced contact hypersensitivity response in mice lacking TNF receptor p75.

Epidermal Langerhans cells (LC) belong to the dendritic cell family and represent the major APC within the skin. LC capture epicutaneous Ag, migrate into regional lymph nodes, and present Ag to T cells, thereby initiating primary immune response. The migratory properties of LC are an essential component of their function. The molecular mechanisms responsible for LC migration are far less defined. However, evidence has been accumulating to suggest that TNF-alpha, a major proinflammatory cytokine, plays an important role in promoting DC migration. To confirm the role of TNF-alpha in LC migration and to examine which type of TNF receptor signaling is involved in such an event, we utilized gene-targeted knockout mice lacking TNF receptor p55 or p75. The migration of LC was assessed by examining the frequency of hapten-bearing cells in draining lymph nodes following hapten FITC painting, and the accumulation of dendritic cells in draining lymph nodes after intradermal injection of TNF-alpha. While LC migration was normal in p55-deficient mice, the migration was markedly depressed in p75-deficient mice. Receptor p75-deficient mice also demonstrated a hyporesponsiveness in allergen-induced contact dermatitis, but a normal responsiveness in irritant-induced contact dermatitis. These results suggest that p75-dependent signaling plays a crucial role in the migration of LC and in the initiation of cutaneous immune responses.

Administration, Cutaneous↗
PubMed1998

Migration of lymphoid cells from vaginal epithelium to iliac lymph nodes in relation to vaginal infection by herpes simplex virus type 2.

To determine whether lymphocytes and Langerhans cells in vaginal epithelium are migratory, we stained mouse vaginal epithelium, including its lymphoid cells, by intraluminal administration of H33342, a fluorescent, vital dye. Stromal staining was superficial, and no free dye reached the iliac lymph nodes. The numbers and phenotypes of H33342-stained cells that migrated from the vagina to the iliac lymph nodes during the next 48 h were determined in four groups: normal mice, mice infected intravaginally with wild-type herpes simplex virus type 2 (HSV-2), mice that were immune to vaginal HSV-2 infection, and immune mice that received vaginal challenge with HSV-2. H33342-stained cells migrated from the vaginal epithelium to the iliac lymph nodes in all groups and were mainly Thy-1.2+ cells and B220+ cells. The number of migrating Thy-1.2+ cells was similar to the sum of CD4+ and CD8+ cells in all groups and was not significantly different from the number of CD44+ cells, suggesting that most of the migrating T cells were memory cells. B lymphocytes comprised 31, 32, 43, and 68% of the migrating cells in the four groups, respectively. We found no evidence that Langerhans cells or macrophages were migrating. Thus, most MHC class II+ cells in all groups were accounted for by B cells, and migrating cells did not express B7.1 or F4/80 or exhibit indented nuclei or dendritic processes. We suggest that the migrating T cells and B cells probably belonged to a pool of lymphocytes that recirculates from blood to tissues and back to the lymph nodes via their afferent lymphatics.

Animals↗
PubMed1998

G protein-mediated inhibition of neuronal migration requires calcium influx.

Neuronal migration is an essential feature of the developing nervous system, but the intracellular signaling mechanisms that regulate this process are poorly understood. During the formation of the enteric nervous system (ENS) in the moth Manduca sexta, the migration of an identified set of neurons (the EP cells) is regulated in part by the heterotrimeric guanyl-nucleotide binding protein (G protein) Goalpha. Using an in vivo culture preparation for developing embryos that allows direct access to the ENS, we have shown that EP cell migration is similarly regulated by intracellular Ca2+; treatments that increased intracellular Ca2+ inhibited the migratory process, whereas buffering intracellular Ca2+ induced aberrant migration onto inappropriate pathways. Imaging the spontaneous changes in intracellular Ca2+ within individual EP cells showed that actively migrating neurons exhibited only small fluctuations in intracellular Ca2+. In contrast, neurons that had reached the end of migration displayed large, transient Ca2+ spikes. Similar Ca2+ spikes were induced in the EP cells by G protein stimulation, an effect that was reversed by removal of external Ca2+. Stimulation of Go in individual EP cells (by injection of either activated Goalpha subunits or mastoparan) also inhibited migration in a Ca2+-dependent manner. These results suggest that the regulation of neuronal migration by G proteins involves a Ca2+-dependent process requiring Ca2+ influx.

Animals↗
PubMed1998

Effects of PDGF on the migration of rabbit corneal fibroblasts and epithelial cells.

PURPOSE: We investigated the effects of human platelet-derived growth factor (PDGF) isomers on the migration of rabbit corneal fibroblasts and epithelial cells in the presence or absence of fibronectin (FN). METHODS: A modified Boyden's chamber method was used to detect cell migration. Cells placed in the inner chamber were incubated with PDGF in the outer chamber at 37 degrees C at 24 h. In addition, epithelial cells were incubated in the presence or absence of FN. The migrated cells were stained and the cell number counted under a microscope. Checkerboard analysis was used to distinguish chemotaxis from chemokinesis. RESULTS: Natural PDGF and PDGF-BB enhanced the migration of corneal fibroblasts, whereas PDGF-AA did not. As for corneal epithelial cells, all the isomers of PDGF enhanced the migration, but only in the presence of FN, as in the absence of FN or at a low concentration gradient of FN, there was no enhanced cell migration. A checkerboard assay demonstrated that PDGF-BB had a chemotactic effect on the migration of corneal fibroblasts and epithelial cells, whereas PDGF-AA had a chemotactic effect on only corneal epithelial cells. CONCLUSION: These results suggest that PDGF is involved in corneal wound healing by stimulating the migration of corneal epithelial cells in the presence of FN and fibroblasts.

Animals↗