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PubMed2004

Intracellular calcium transients are necessary for platelet-derived growth factor but not extracellular matrix protein-induced vascular smooth muscle cell migration.

PURPOSE: Vascular smooth muscle cell (SMC) migration is a critical component of the hyperplastic response that leads to recurrent stenosis after interventions to treat arterial occlusive disease. We investigated the relationship between intracellular calcium ([Ca(2+)](i)) and migration of vascular SMCs in response to platelet-derived growth factor (PDGF) and extracellular matrix (ECM) proteins. METHODS: Human saphenous vein SMCs were used for all experiments. SMC migration in response to agonists was measured with a microchemotaxis assay. A standard fluorimetric assay was used to assess changes in [Ca(2+)](i) in response to the various combinations of growth factors and ECM proteins. RESULTS: The calcium ionophore A23187 produced a rapid rise in [Ca(2+)](i) and a corresponding 60% increase in SMC migration, whereas chelation of [Ca(2+)](i) with BAPTA (1,2-bis [aminophenoxy] ethane-N,N,N',N'-tetraacetic acid) produced a fivefold decrease in PDGF-induced chemotaxis, suggesting that [Ca(2+)](i) is both sufficient and necessary for SMC migration. Stimulation of SMCs with PDGF produced an early peak followed by a late plateau in [Ca(2+)](i). To establish a relationship between temporal fluctuations in [Ca(2+)](i) and SMC migration, SMCs were pretreated with caffeine and ryanadine, which eliminated the initial peak but not the late plateau in [Ca(2+)](i), and had no effect on chemotaxis in response to PDGF. Incubation of SMCs with nickel chloride eliminated the late plateau, but had no effect on the initial peak in [Ca(2+)](i), and reduced PDGF-stimulated migration by fivefold. We then evaluated the role of calcium in SMC migration induced by ECM proteins such as laminin, fibronectin, and collagen types I and IV. All four matrix proteins stimulated SMC migration, but none produced an elevation in [Ca(2+)](i). Moreover, preincubation of SMCs with caffeine and ryanadine or nickel chloride had no effect on ECM protein-induced chemotaxis. CONCLUSION: [Ca(2+)](i) transients are necessary for PDGF but not ECM protein-induced SMC chemotaxis. Moreover, the ability of PDGF to stimulate vascular SMC migration appears dependent on influx of extracellular calcium through membrane channels. CLINICAL RELEVANCE: Recurrent stenosis after angioplasty or surgical bypass remains a significant challenge in treating vascular occlusive disease. In addition to growth factors, extracellular matrix (ECM) proteins may be potent agonists of this process. In this study we show that the influx of extracellular calcium is an important mechanism for platelet-derived growth factor-induced smooth muscle cell migration but not ECM-induced migration. Of note, in clinical trials calcium channel blockers failed to inhibit recurrent stenosis. Our data provide mechanistic insight to help explain this negative outcome in that therapies designed to inhibit restenosis depend on the effects of both growth factors and ECM proteins.

Calcimycin↗
PubMed2000

Quantitative analysis of the regulation of leukocyte chemosensory migration by a vascular prosthetic biomaterial.

The need for improved, infection-resistant vascular biomaterials calls for more objective evaluation of the immune pathophysiology of implantable prosthetic materials. In this study we have developed a new strategy to quantitatively characterize population-averaged responses of immune cell migration on vascular prosthetic materials. This approach, incorporating a chemokinetically regulated "biomaterial-gel" sandwich configuration, was applied to quantify both random and directed modes of the chemosensory migration of human neutrophil leukocytes on expanded polytetrafluoroethylene (ePTFE). Our studies show that (a) microporous, synthetic materials like ePTFE suppress the basal rate of random cell migration relative to that reported on non-porous control surfaces; (b) stimulation with chemoattractant (formyl peptide) can significantly elevate rates of random and directed migration on ePTFE; and (c) protein conditioning of ePTFE with albumin or immunoglobulin G can differentially modulate the rates and relative proportion of random and directional components of leukocyte migration response to chemoattractant. This, to our knowledge, is the first objective quantitation of chemokinetically regulated cell migration on implantable prosthetic materials.

Journal Article↗
PubMed2003

The anti-inflammatory effect of bee venom stimulation in a mouse air pouch model is mediated by adrenal medullary activity.

Cutaneous electrical or chemical stimulation can produce an anti-inflammatory effect, which is dependent on adrenal medullary-sympathetic activation. We have previously shown that peripheral injection of bee venom (BV) also produces a significant anti-inflammatory effect that is neurally mediated. In the present study, we examined whether this anti-inflammatory effect is also dependent on the adrenal gland using the mouse inflammatory air pouch model. Subcutaneous (s.c.) BV injection produced a marked suppression of leucocyte migration and tumour necrosis factor (TNF)-alpha concentration induced by zymosan injection into the air pouch. The role of the adrenal gland in this suppression was evaluated in adrenalectomized mice. Adrenalectomy significantly reversed the suppression of leucocyte migration and TNF-alpha elevation caused by BV. Serum concentrations of corticosteroid were increased in mice with zymosan-induced air-pouch inflammation and this increase was reduced by BV administration, suggesting that adrenal corticosteroid release is not involved in mediating the anti-inflammatory effects of BV. To test this hypothesis, the corticosteroid receptor antagonist (RU486) was administered and found not to affect the BV-induced inhibition of leucocyte migration. By contrast, pretreatment with the beta-adrenergic antagonist propranolol reversed the BV-induced inhibitory effect on leucocyte migration. These results suggest that the anti-inflammatory effect of s.c. BV administration is mediated in part by the release of catecholamines from the adrenal medulla.

Adrenal Medulla↗
PubMed1989

Changes in plasma and pituitary levels of prolactin in the toad, Bufo japonicus, throughout the year with special reference to the breeding migration.

Monthly surveys of the plasma prolactin level in Bufo japonicus at two localities, one in Tokyo and the other in Saitama Prefecture, revealed that the level was highest during the month of breeding in early spring with an additional peak recognized in autumn. The level was lowest during the winter torpid period before breeding and during the spring torpid period after breeding. The pituitary prolactin content observed in Tokyo also showed an annual cycle similar to the plasma prolactin, except that the content in winter was higher than that in summer. A further precise survey of the plasma prolactin level before and during the breeding period revealed that the level in male toads migrating toward the pond for breeding was as low as the level in torpid toads, and also that the level was elevated in only about 50% of migrating female toads. In the pond, almost all female and male toads showed high plasma prolactin levels. Soon after the females finished breeding and returned to land, the level declined to the baseline without exception. In contrast, many males retained high levels on land. The present results indicate that prolactin is not a water drive factor, at least in B. japonicus. Prolactin may, however, play a role in toad osmoregulation in water. There is a possibility that the high prolactin level in some of the migrating female toads is related to oviductal secretion, as some female toads ovulate during migration.

Acclimatization↗
PubMed1998

Differential response of cortical plate and ventricular zone cells to GABA as a migration stimulus.

A microdissection technique was used to separate differentiated cortical plate (cp) cells from immature ventricular zone cells (vz) in the rat embryonic cortex. The cp population contained >85% neurons (TUJ1(+)), whereas the vz population contained approximately 60% precursors (nestin+ only). The chemotropic response of each population was analyzed in vitro, using an established microchemotaxis assay. Micromolar GABA (1-5 microM) stimulated the motility of cp neurons expressing glutamic acid decarboxylase (GAD), the rate-limiting enzyme in GABA synthesis. In contrast, femtomolar GABA (500 fM) directed a subset of GAD- vz neurons to migrate. Thus, the two GABA concentrations evoked the motility of phenotypically distinct populations derived from different anatomical regions. Pertussis toxin (PTX) blocked GABA-induced migration, indicating that chemotropic signals involve G-protein activation. Depolarization by micromolar muscimol, elevated [K+]o, or micromolar glutamate arrested migration to GABA or GABA mimetics, indicating that migration is inhibited in the presence of excitatory stimuli. These results suggest that GABA, a single ligand, can promote motility via G-protein activation and arrest attractant-induced migration via GABAA receptor-mediated depolarization.

Animals↗
PubMed1977

[Changes in the electric charge of blood lymphocyte populations after secondary immunization with tetanus antitoxin in man].

The electrophoretic mobility of circulating lymphocytes has been studied in normal human subjects after immunization by tetanus toxoid. The mean migration speed was shown to increase, particularly two and three days after secondary immunization. This increase appeared to be due to the elevation of percentage of T cells migrating at 1.20 and 1.35 micrometer. sec.-1v.-1 cm. (active rosettes-forming cells), with a decrease of the percentage of B cells and T lymphocytes migrating at 1.10 micrometer. sec.-1v.-1 cm. The return to the anterior status was observed between day 4 and 8 after immunization.

Electrophoresis↗
PubMed1986

Murine neutrophil migration during the course of an intra-abdominal abscess.

Studies of neutrophil migration in heterogeneous groups of septic patients have reported elevated, normal, and depressed neutrophil mobility. This experiment, conducted in a standardized murine population, measured neutrophil migration under agarose during the course of a chronic intra-abdominal abscess initiated by cecal ligation. Compared with both control (unoperated) and sham celiotomy mice, those mice with an abdominal abscess showed elevations of 22% and 14% of directed and random migration, respectively, at 48 hours. They had 30% to 40% decreases in these functions at days 4 through 10. Murine neutrophil migratory response during the course of an intra-abdominal abscess consisted therefore of an early elevation followed by a prolonged depression. Such a biphasic response could underlie the variable findings of neutrophil studies in septic patients. This model could be further applied to the study of the effects of chemotherapy and immunologic adjuvants on abscess course and neutrophil function, as well as to the study of the mechanisms of neutrophil response to sepsis.

Abdomen↗
PubMed2006

Airway smooth muscle and mast cell-derived CC chemokine ligand 19 mediate airway smooth muscle migration in asthma.

RATIONALE: Airway smooth muscle (ASM) hyperplasia is a feature of asthma, and increases with disease severity. We hypothesized that this results from migration of ASM or progenitors in response to chemokines derived from ASM or mast cells within the ASM bundle. OBJECTIVES: To examine expression of the chemokine receptor, CC chemokine receptor (CCR) 7, in vivo by ASM in patients with asthma and healthy control subjects, and by primary cultures of ASM and fibroblasts; to define expression of its ligands, CC chemokine ligand (CCL) 19 and CCL21, in bronchial biopsies, and primary cultures of ASM and mast cells; and to investigate CCR7's role in ASM migration and repair. METHODS: ASM was isolated from bronchoscopy and resection tissue. Receptor and chemokine expression was examined by immunohistochemistry, immunofluorescence, flow cytometry, ELISA, and reverse transcriptase-polymerase chain reaction. CCR7 function was examined by intracellular calcium measurements, chemotaxis, wound healing assays, and measurement of cell proliferation. MEASUREMENTS AND MAIN RESULTS: ASM, myofibroblasts, and fibroblasts expressed CCR7. CCL19, but not CCL21, was highly expressed in bronchial biopsies by mast cells and vessels in asthma of all severities, ASM in severe disease, and ex vivo ASM and mast cells. ASM CCR7 activation by CCL19-mediated intracellular calcium elevation and concentration-dependent migration, but not proliferation. Importantly, mast cell and ASM-derived CCL19 mediated ASM migration and repair. CONCLUSIONS: The CCL19/CCR7 axis may play an important role in the development of ASM hyperplasia in asthma.

Asthma↗
PubMedDate not supplied

Assessing and managing exposure from arsenic in CCA-treated wood play structures.

BACKGROUND: Chromated copper arsenate (CCA)-treated wood has been widely used for outdoor play structures. There is a growing scientific concern about children's exposure to the arsenic that leaches from these structures. The purpose of this study was to measure arsenic from CCA-treated wood play structures owned by the City of Toronto to guide an appropriate exposure reduction strategy. METHODS: In the fall of 2002, 4 soil and 2 wood surface samples (dislodgeable arsenic) were collected from 217 play structures and analyzed for total arsenic content. Soil arsenic concentrations were compared to the federal soil guideline of 12 microg/g. Dislodgeable arsenic concentrations were compared to a Toronto Public Health-derived interim action level of 100 microg/100 cm2. RESULTS: Soil arsenic levels in samples taken from within one metre of CCA-treated wood were low (mean 2.1; range 0.5-10 microg/g). However, the means of the arsenic level in the composite soil samples taken from beneath an elevated platform were significantly greater (p<0.01) than the background soil sample and soil from within one metre of the CCA-treated wood (mean 20.3; range 12.4-47.5 microg/g). Composite soil samples exceeded the federal soil guideline of 12 microg/g at 32 play structures. Dislodgeable arsenic values varied widely (mean 41.9 microg/100 cm2; non-detectable to 521.5 microg/100 cm2). 32 play structures had dislodgeable arsenic levels that exceeded the interim action level. Mean arsenic concentrations on vertical surfaces were significantly higher than on horizontal surfaces (p<0.01). DISCUSSION: Our soil analysis indicates that arsenic does not migrate laterally but accumulates under elevated platforms at levels that can exceed the soil guideline. Dislodgeable arsenic values varied greatly and were not a useful predictor of soil arsenic (R2 = 0.0015).

Arsenic↗
PubMed2004

Arginine stimulates intestinal cell migration through a focal adhesion kinase dependent mechanism.

BACKGROUND: L-Arginine is a nutritional supplement that may be useful for promoting intestinal repair. Arginine is metabolised by the oxidative deiminase pathway to form nitric oxide (NO) and by the arginase pathway to yield ornithine and polyamines. AIMS: To determine if arginine stimulates restitution via activation of NO synthesis and/or polyamine synthesis. METHODS: We determined the effects of arginine on cultured intestinal cell migration, NO production, polyamine levels, and activation of focal adhesion kinase, a key mediator of cell migration. RESULTS: Arginine increased the rate of cell migration in a dose dependent biphasic manner, and was additive with bovine serum concentrate (BSC). Arginine and an NO donor activated focal adhesion kinase (a tyrosine kinase which localises to cell matrix contacts and mediates beta1 integrin signalling) after wounding. Arginine stimulated cell migration was dependent on focal adhesion kinase (FAK) signalling, as demonstrated using adenovirus mediated transfection with a kinase negative mutant of FAK. Arginine stimulated migration was dependent on NO production and was blocked by NO synthase inhibitors. Arginine dependent migration required synthesis of polyamines but elevating extracellular arginine concentration above 0.4 mM did not enhance cellular polyamine levels. CONCLUSIONS: These results showed that L-arginine stimulates cell migration through NO and FAK dependent pathways and that combination therapy with arginine and BSC may enhance intestinal restitution via separate and convergent pathways.

Animals↗
PubMed2001

Temperature and pH studies of short tandem repeat systems using capillary electrophoresis at elevated pH.

The DNA secondary structure can affect the migration time and precision of DNA separations in the physical gels used in capillary electrophoresis (CE). To counteract these effects, DNA typing is performed using elevated temperatures (60 degrees C) and high concentrations (7 M) of urea. These conditions affect the precision and lifetime of the analysis. To better understand the effects of these conditions on the reproducibility of DNA migration, we examined the effects of temperature and pH on short tandem repeat (STR) analysis using the PE/ABI 310 Genetic Analyzer. Separations were performed using the Profiler + multiplex system, a set of coamplified STRs with a 4-base repeat motif, labeled at the 5'-end using fluorescent dyes. The analytical separations were obtained using a commercial buffer at pH 8 and an experimental buffer consisting of 3% hydroxyethylcellulose at pH settings ranging from 8-12. Multichannel laser-induced fluorescence detection was used. Temperatures were examined from 30-70 degrees C. The results demonstrate the fact that highly efficient separations can be carried out at alkaline pH. In addition, improvements in temperature stability were seen when compared to results at lower pH. However, high concentrations of urea were found to be necessary to achieve optimal resolution.

Alleles↗
PubMed2004

Extracellular HMGB1, a signal of tissue damage, induces mesoangioblast migration and proliferation.

High mobility group box 1 (HMGB1) is an abundant chromatin protein that acts as a cytokine when released in the extracellular milieu by necrotic and inflammatory cells. Here, we show that extracellular HMGB1 and its receptor for advanced glycation end products (RAGE) induce both migration and proliferation of vessel-associated stem cells (mesoangioblasts), and thus may play a role in muscle tissue regeneration. In vitro, HMGB1 induces migration and proliferation of both adult and embryonic mesoangioblasts, and disrupts the barrier function of endothelial monolayers. In living mice, mesoangioblasts injected into the femoral artery migrate close to HMGB1-loaded heparin-Sepharose beads implanted in healthy muscle, but are unresponsive to control beads. Interestingly, alpha-sarcoglycan null dystrophic muscle contains elevated levels of HMGB1; however, mesoangioblasts migrate into dystrophic muscle even if their RAGE receptor is disabled. This implies that the HMGB1-RAGE interaction is sufficient, but not necessary, for mesoangioblast homing; a different pathway might coexist. Although the role of endogenous HMGB1 in the reconstruction of dystrophic muscle remains to be clarified, injected HMGB1 may be used to promote tissue regeneration.

Animals↗
PubMed2003

Chemotactic role of neurotropin 3 in the embryonic testis that facilitates male sex determination.

The first morphological event after initiation of male sex determination is seminiferous cord formation in the embryonic testis. Cord formation requires migration of pre-peritubular myoid cells from the adjacent mesonephros. The embryonic Sertoli cells are the first testicular cells to differentiate and have been shown to express neurotropin-3 (NT3), which can act on high-affinity trkC receptors expressed on migrating mesonephros cells. NT3 expression is elevated in the embryonic testis during the time of seminiferous cord formation. A trkC receptor tyrophostin inhibitor, AG879, was found to inhibit seminiferous cord formation and mesonephros cell migration. Beads containing NT3 were found to directly promote mesonephros cell migration into the gonad. Beads containing other growth factors such as epidermal growth factor (EGF) did not influence cell migration. At male sex determination the SRY gene promotes testis development and the expression of downstream sex differentiation genes such as SOX-9. Inhibition of NT3 actions caused a reduction in the expression of SOX-9. Combined observations suggest that when male sex determination is initiated, the developing Sertoli cells express NT3 as a chemotactic agent for migrating mesonephros cells, which are essential to promote embryonic testis cord formation and influence downstream male sex differentiation.

Animals↗
PubMed2000

Macrophage migration inhibitory factor up-regulates expression of matrix metalloproteinases in synovial fibroblasts of rheumatoid arthritis.

Neutral matrix metalloproteinases (MMPs) are responsible for the pathological features of rheumatoid arthritis (RA) such as degradation of cartilage. We herein show the up-regulation of MMP-1 (interstitial collagenase) and MMP-3 (stromelysin) mRNAs of cultured synovial fibroblasts retrieved from rheumatoid arthritis (RA) patients in response to macrophage migration inhibitory factor (MIF). The elevation of MMP-1 and MMP-3 mRNA was dose-dependent and started at 6 h post-stimulation by MIF, reached the maximum level at 24 h, and was sustained at least up to 36 h. Interleukin (IL)-1beta mRNA was also up-regulated by MIF. These events were preceded by up-regulation of c-jun and c-fos mRNA. Tissue inhibitor of metalloproteinase (TIMP)-1, a common inhibitor of these proteases, was slightly up-regulated by MIF. Similarly, mRNA up-regulation of MMP-1 and MMP-3 was observed in the synovial fibroblasts of patients with osteoarthritis. However, their expression levels were much lower than those of RA synovial fibroblasts. The mRNA up-regulation by MIF was inhibited by the tyrosine kinase inhibitors genestein and herbimycin A, as well as the protein kinase C inhibitors staurosporine and H-7. On the other hand, the inhibition was not seen after the addition of the cyclic AMP-dependent kinase inhibitor, H-8. The mRNA up-regulation of MMPs was also inhibited by curcumin, an inhibitor of transcription factor AP-1, whereas interleukin-1 receptor antagonist, an IL-1 receptor antagonist, failed to inhibit the mRNA up-regulation. Considering these results, it is suggested that 1) MIF plays an important role in the tissue destruction of rheumatoid joints via induction of the proteinases, and 2) MIF up-regulates MMP-1 and MMP-3 via tyrosine kinase-, protein kinase C-, and AP-1- dependent pathways, bypassing IL-1beta signal transduction.

Arthritis, Rheumatoid↗
PubMed2003

Activation of c-Met in colorectal carcinoma cells leads to constitutive association of tyrosine-phosphorylated beta-catenin.

Increased expression and/or activity of c-Met, the receptor protein tyrosine kinase for hepatocyte growth factor/scatter factor, occurs commonly during colon tumor progression. To examine potential roles for c-Met in promoting metastasis, we compared the colon tumor cell line KM12C with low metastatic potential to the isogenic variants KM,12L4 and KM12SM with high metastatic potential. KM12C cells express c-Met with low levels of tyrosine phosphorylation in the absence of HGF. The high metastatic cells express a c-Met that is constitutively tyrosine phosphorylated, they have increased colony formation, and are minimally responsive to HGF relative to the parental cells. Tyrosine-phosphorylated beta-catenin was constitutively associated with c-Met in the more metastatic cells, but was inducible only after HGF addition in the less metastatic cells. Functions mediated by beta-catenin, including cell-cell adhesion and migration, and activation of the tcf (T-cell factor) family of transcription factors, were also elevated in the more metastatic KM12SM and L4 cells. Furthermore, analysis of the known tcf transcriptional target genes, cyclin D1, c-Myc, and uPAR, demonstrated increased expression in the high metastatic cells, correlating with the levels of tcf activity. Collectively, these results suggest that endogenous activation of c-Met in highly metastatic KM12SM CRC cells results in increased survival and growth under anchorage independent conditions, increased in vitro migration, and elevated levels of tcf target genes. Thus, beta-catenin association with activated c-Met may contribute to a more aggressive liver metastatic phenotype of these cells.

Blotting, Western↗
PubMed1985

Plasma motilin concentration and interdigestive migrating motor complex in diabetic gastroparesis: effect of metoclopramide.

The objective of this study is to determine whether abnormal rhythm and amplitude of the oscillation in plasma motilin concentration are responsible for the abnormal motility observed in patients with diabetic gastroparesis. We also investigated the effect of metoclopramide on plasma motilin concentration and gastrointestinal motility in these patients. In healthy controls, basal plasma motilin concentration fluctuated in phase with the interdigestive migrating motor complex. All patients with diabetic gastroparesis did not have antral phase III activities and had significantly higher basal motilin concentrations, which maintained a normal oscillatory pattern. Administration of metoclopramide initiated antral phase III activities in healthy controls and in patients with diabetic gastroparesis. These were accompanied by a concurrent rise in plasma motilin concentration in healthy controls, contrasting with a fall in plasma motilin concentrations in patients with diabetic gastroparesis. We conclude that diabetic gastroparesis is associated with absence of antral interdigestive migrating motor complex and with elevated plasma motilin concentration with normal cyclic fluctuations. Our studies also show that metoclopramide initiates antral phase III activities in diabetic gastroparesis independent of plasma motilin concentration.

Adolescent↗
PubMed1998

Gene amplification and increased expression of the reduced folate carrier in transport elevated K562 cells.

The molecular bases for the 6-fold elevated methotrexate transport capacity of K562.4CF cells (Matherly et al., Cancer Res. 51: 3420-3426, 1991) were studied with reduced folate carrier (RFC) cDNA, genomic, and antibody probes. Southern analysis showed that RFC gene copies were increased (approximately 4- to 5-fold) in K562.4CF over wild-type K562 cells. Fluorescence in situ hybridization using a genomic RFC probe confirmed the localization of the RFC gene to the q-arm of chromosome 21. In K562.4CF cells, the frequent loss of a normal copy of chromosome 21 (61% of metaphases) was accompanied by RFC gene amplification and translocations of amplified RFC gene fragments to several (2 to 6) different chromosomal loci not seen in wild-type cells. Particularly intense RFC signals were mapped to homogeneously staining regions in chromosomes 2 and 15. Increased RFC gene copies were accompanied by a similar increase in the major 3.1 kb RFC transcript by northern blotting and an approximately 7-fold elevated level of the broadly migrating (80-95 kDa) RFC protein on a western blot probed with an RFC C-terminal peptide antibody. These results demonstrate that selection of cells with a growth-limiting concentration of reduced folates (0.4 nM of leucovorin) is sufficient to promote chromosomal aberrations, including gene amplification and translocations that result in increased RFC expression and folate transport.

Blotting, Western↗