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PubMed2004

A vertebrate crossveinless 2 homologue modulates BMP activity and neural crest cell migration.

Previous work has revealed that proteins that bind to bone morphogenetic proteins (BMPs) and inhibit their signalling have a crucial role in the spatial and temporal regulation of cell differentiation and cell migration by BMPs. We have identified a chick homologue of crossveinless 2, a Drosophila gene that was identified in genetic studies as a promoter of BMP-like signalling. Chick Cv-2 has a conserved structure of five cysteine-rich repeats similar to those found in several BMP antagonists, and a C-terminal Von Willebrand type D domain. Cv-2 is expressed in the chick embryo in a number of tissues at sites at which elevated BMP signalling is required. One such site of expression is premigratory neural crest, in which at trunk levels threshold levels of BMP activity are required to initiate cell migration. We show that, when overexpressed, Cv-2 can weakly antagonise BMP4 activity in Xenopus embryos, but that in other in vitro assays Cv-2 can increase the activity of co-expressed BMP4. Furthermore, we find that increased expression of Cv-2 causes premature onset of trunk neural crest cell migration in the chick embryo, indicative of Cv-2 acting to promote BMP activity at an endogenous site of expression. We therefore propose that BMP signalling is modulated both by antagonists and by Cv-2 that acts to elevate BMP activity.

Amino Acid Sequence↗
PubMed2004

Statins contribute to enhancement of the number and the function of endothelial progenitor cells from peripheral blood.

The aim of the present study was to investigate whether fluvastatin augments the number of endothelial progenitor cells (EPCs), and promotes EPCs proliferation, migration and adhesion. Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation. The cells were then plated on fibronectin-coated culture dishes. After being cultured for 7 d, the attached cells were stimulated with fluvastatin (final concentrations: 0.01, 0.1, 1, 10 micromol/L), simvastatin (1 micromol/L) or a vehicle for the respective time points (6, 12, 24 and 48 h). EPCs were characterized as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining under a laser scanning confocal microscope. EPCs were further documented by demonstrating the expression of KDR, VEGFR-2 and AC133 with flow cytometry. EPCs proliferation, migration and in vitro vasculogenesis activity were assayed by MTT assay, modified Boyden chamber assay and in vitro vasculogenesis kit, respectively. EPCs adhesion assay was performed by replating it on fibronectin-coated dishes, and the adherent cells were then counted. In addition, we also studied EPCs culture assay of peripheral blood from fluvastatin-treated animals in vivo. Incubation of isolated human MNCs with fluvastatin dose- and time-dependently increased the number of EPCs, while reached the maximum 24 h after the administration at 1 micromol/L, (2.5-fold increase, P<0.05). Moreover, treatment of rats with fluvastatins elevated the number of EPCs (3-fold increase, P<0.05), thus extending the in vitro data. In addition, fluvastatin also promoted EPC proliferation, migration, adhesion and in vitro vasculogenesis in a concentration-dependent manner. The effects of fluvastatin on EPCs were compared with those of simvastatin at the same concentration (1 micromol/L), with a result of no statistical difference. The results of the present study define a novel mechanism of the action of statins: the augmentation of EPCs with enhanced functional activity.

Cell Adhesion↗
PubMed2006

BMP signaling regulates PGC numbers and motility in organ culture.

Members of the bone morphogenetic protein (BMP) family play diverse roles in multiple developmental processes. However, in the mouse, mutations in many BMPs, BMP receptors and signaling components result in early embryonic lethality making it difficult to analyze the role of these factors during organogenesis or tissue homeostasis in the adult. To bypass this early lethality, we used an organ culture system to study the role of BMPs during primordial germ cell (PGC) migration. PGCs are the embryonic precursors of the sperm and eggs. BMPs induce formation of primordial germ cells within the proximal epiblast of embryonic day 7.5 (E7.5) mouse embryos. PGCs then migrate via the gut to arrive at the developing gonads by E10.5. Addition of BMP4 or the BMP-antagonist Noggin to transverse slices dissected from E9.5 embryos elevated PGC numbers or reduced PGC numbers, respectively. Noggin treatment also slowed and randomized PGC movements, resulting in a failure of PGCs to colonize the urogenital ridges (UGRs). Based on p-Smad1/5/8 staining, migratory PGCs do not respond to endogenous BMPs. Instead, the somatic cells of the urogenital ridges exhibit elevated p-Smad1/5/8 staining revealing active BMP signaling within the UGRs. Noggin treatment abrogated p-Smad staining within the UGRs and blocked localized expression of Kitl, a cytokine known to regulate the survival and motility of PGCs and Id1, a transcription factor expressed within the UGRs. We propose that BMP signaling regulates PGC migration by controlling gene expression within the somatic cells along the migration route and within the genital ridges.

Animals↗
PubMed2002

Sources and migration of plutonium in groundwater at the Savannah River site.

The isotopic composition, size distribution, and redox speciation of plutonium (Pu) in the groundwater in the vicinity of the F-area seepage basins at the U.S. Department of Energy Savannah River Site (SRS) were examined. A low 240Pu/239Pu ratio in the upstream control well signifies a Pu source otherthan global fallout and indicates reactor-produced Pu. Elevated 240Pu/239Pu atom ratios downstream from the seepage basins are due to the decay of transplutonium isotopes, mainly 244Cm to 240Pu, which were generated at the SRS. Evidence suggests that the migration of basin-released Pu isotopes is minor. Rather, it is the transplutonium isotopes that migrate preferentially downstream and in the process decay to yield progeny Pu isotopes. Size fractionation studies with cross-flow ultrafiltration show that <4% of the 239Pu or 240Pu is found in the colloidal fraction, a finding that is consistent with the higher Pu oxidation states observed in the SRS groundwater. The observation of a low abundance of colloid-associated Pu in SRS groundwater cannot be extrapolated to all sites, but is in contrast to the conclusions of prior groundwater Pu studies at the SRS and elsewhere. This work is unique in its application of a novel combination of sampling and processing protocols as well as its use of thermal ionization mass spectrometry for the detection of Pu isotopes. This allows quantification of the Pu source terms and better determination of the ambient Pu size and redox speciation representative of in situ conditions.

Colloids↗
PubMed1994

Long-term impaired neutrophil migration in mice overexpressing human interleukin-8.

The proinflammatory chemokine interleukin-8 (IL-8/NAP-1) has been implicated in recruiting neutrophils to sites of acute and chronic tissue inflammation. In transgenic mice, elevated serum IL-8 levels ranging from 1 to 118 ng/ml were correlated with proportional increases in circulating neutrophils and proportional decreases in L-selectin expression on the surface of blood neutrophils. No change in the expression of the beta 2-integrins Mac-1 and LFA-1 was apparent on peripheral blood neutrophils of the IL-8 transgenic mice. Additionally, L-selectin expression on bone marrow neutrophils and neutrophil precursors was normal in all transgenic lines. IL-8 transgenic mice demonstrated an accumulation of neutrophils in the microcirculation of the lung, liver and spleen. Moreover, there was no evidence of neutrophil extravasation, plasma exudation or tissue damage in any IL-8 transgenic mice. Neutrophil migration into the inflamed peritoneal cavity was severely inhibited in IL-8 transgenic mice, but not in nontransgenic littermates. The IL-8 transgenic mice should serve as useful models for studying the putative role of neutrophils in mediating tissue damage in models of inflammation, such as hepatic ischemia and reperfusion injury, cecal puncture and ligation, and glomerulonephritis.

Animals↗
PubMed2000

Mechanisms of progenitor maturation are conserved in the striatum and cortex.

We recently reported that developmental changes in the expression of epidermal growth factor receptors (EGFRs) by cortical progenitor cells regulate their fate and migration. Higher levels of EGFRs are expressed by later embryonic progenitor cells and are required for several responses to EGF family ligands, including astrocyte differentiation and migration. Progenitor cells in the ganglionic eminence (GE), the forerunner of the striatum, also exhibit a developmental increase in EGFR expression. The striatum differs from the cortex in several respects, including cytoarchitecture, the timing of changes in EGFRs, and the level of transforming growth factor-alpha (TGFalpha) expression. To determine whether signaling mediated by EGFRs in GE progenitors regulates their fate and migration as observed in cortex, we used a retrovirus to increase EGFR expression in embryonic GE progenitor cells prematurely. As in cortex, premature elevation of EGFRs promoted the departure of GE progenitors from the ventricular zone and their differentiation into astrocytes. Settling patterns of infected cells in the striatum, however, differed from the patterns observed in cortex. In addition, the extent of premature astrocyte differentiation reached similar levels in striatal cells, even in the presence of greater endogenous TGFalpha. These findings suggest that additional factors play an important role in modulating EGFR-mediated changes in cell fate. Together with previous studies in cortex, these observations in the striatum indicate that a conserved mechanism involving developmental changes in EGFR expression regulates cell fate and the timing of migration.

Animals↗
PubMed2006

cAMP elevating agents suppress secretory phospholipase A(2)-induced matrix metalloproteinase-2 activation.

Phospholipase A2 proteins are major regulators of the arachidonic acid cascade and are involved in various cellular responses. Previously, we reported that group IB PLA2 proteins stimulate MMP-2 activation and subsequent cell migration. Here, we describe a novel mechanism whereby sPLA2-induced proMMP-2 activation is regulated by intracellular cAMP in HT1080 cells, although sPLA2 itself had no effect on the regulation of cAMP levels. Exogenous dibutyryl cAMP (a cAMP analogue) strongly inhibited proMMP-2 activation, and cAMP elevating agents, namely, cholera toxin (a Gs activator) and forskolin (an adenylyl cyclase activator), abrogated basal and sPLA2-induced proMMP-2 activation. We also found that the down-regulation of TIMP-2 expression and extracellular signal-regulated kinase (ERK)1/2 activation by sPLA2 were blocked by increasing the intracellular cAMP level. Taken together, our data indicate that sPLA2-induced proMMP-2 activation is influenced by intracellular cAMP levels via the modulations of TIMP-2 expression and ERK1/2 activation.

Cell Line↗
PubMed1997

Potential roles of osteopontin and alphaVbeta3 integrin in the development of coronary artery restenosis after angioplasty.

Angioplasty procedures are increasingly used to reestablish blood flow in blocked atherosclerotic coronary arteries. A serious complication of these procedures is reocclusion (restenosis), which occurs in 30-50% of patients. Migration of coronary artery smooth muscle cells (CASMCs) to the site of injury caused by angioplasty and subsequent proliferation are suggested mechanisms of reocclusion. Using both cultured human CASMCs and coronary atherectomy tissues, we studied the roles of osteopontin (OPN) and one of its receptors, alphavbeta3 integrin, in the pathogenesis of coronary restenosis. We also measured the plasma levels of OPN before and after angioplasty and determined the effect of exogenous OPN on CASMC migration, extracellular matrix invasion, and proliferation. We found that cultured CASMCs during log phase of growth and smooth muscle cell layer of the coronary atherosclerotic tissues of patients express both OPN mRNA and protein at a significantly elevated level compared with controls. Interestingly, whereas the baseline plasma OPN levels in control samples were virtually undetectable, those in patient plasma were remarkably high. We also found that interaction of OPN with alphavbeta3 integrin, expressed on CASMCs, causes migration, extracellular matrix invasion, and proliferation. These effects were abolished when OPN or alphavbeta3 integrin gene expression in CASMCs was inhibited by specific antisense S-oligonucleotide treatment or OPN-alphavbeta3 interaction was blocked by treatment of CASMCs with antibodies against OPN or alphavbeta3 integrin. Our results demonstrate that OPN and alphavbeta3 integrin play critical roles in regulating cellular functions deemed essential for restenosis. In addition, these results raise the possibility that transient inhibition of OPN gene expression or blocking of OPN-alphavbeta3 interaction may provide a therapeutic approach to preventing restenosis.

Adolescent↗
PubMed2005

Type I collagen and divalent cation shifts disrupt cell-cell adhesion, increase migration, and decrease PTHrP, IL-6, and IL-8 expression in pancreatic cancer cells.

BACKGROUND: We have shown in FG pancreatic cancer cells that alpha2beta1 integrin-mediated type I collagen adhesion decreases parathyroid hormone-related protein (PTHrP), interleukin-6 (IL-6), and interleukin-8 (IL-8) expression, decreases the localization of E-cadherin and beta-catenin in cell-cell contacts, increases cell migration, and increases glycogen synthase kinase 3 (GSK3) and protein kinase B (PKB/Akt) phosphorylation states relative to alpha5beta1 integrin-mediated fibronectin (Fn) adhesion. AIM OF THE STUDY: To extend our observations in FG cells to other pancreatic cancer cell lines, and to determine whether E-cadherin-mediated cell-cell adhesion and its downstream effectors were functionally involved in the ECM-mediated regulation of PTHrP, IL-6, and IL-8. METHODS: We used standard biochemical techniques to determine ECM-specific differences in E-cadherin and beta-catenin localization, GSK3 and PKB/Akt phosphorylation, haptokinetic cell migration, and cytokine expression in pancreatic cancer cells. We also conducted functional studies using pharmacological inhibitors for GSK3 and PKB/Akt, as well as elevated Mg2+/Ca2+ ratios similar to pancreatic juice, and examined their effects on cytokine expression. RESULTS: Differences in E-cadherin and beta-catenin localization along with GSK3 and PKB/Akt phosphorylation occur in multiple pancreatic cancer cell lines, resulting in differences in ECM-mediated haptokinesis and cytokine expression that are generally consistent with previous observations in FG cells. Our functional studies also suggest that E-cadherin-mediated cell-cell adhesion and downstream effectors are involved in PTHrP, IL-6, and IL-8 expression. CONCLUSIONS: These data indicate that alpha2beta1 integrin-mediated type I collagen adhesion disrupts cell-cell adhesion architecture, resulting in increased migration and decreased PTHrP, IL-6, and IL-8 expression in pancreatic cancer cells.

Adenocarcinoma↗
PubMed1986

Zellweger syndrome: diagnostic assays, syndrome delineation, and potential therapy.

Patients with the cerebrohepatorenal syndrome of Zellweger lack peroxisomes and certain peroxisomal enzymes such as dihydroxyacetone phosphate acyltransferase in their tissues. Deficiency of this enzyme, which is necessary for glycerol ether lipid synthesis, provides a biochemical method for recognizing patients with subtle manifestations of Zellweger syndrome and suggests the utility of exogenous ether lipid precursors as a therapeutic strategy for these children. We describe the results of glycerol ether lipid supplementation to two children, one with classic Zellweger syndrome and 9% of control fibroblast dihydroxyacetone phosphate acyltransferase activity, and one with mild facial manifestations, wide sutures, hypotonia, developmental delay, hepatomegaly, peripheral retinal pigmentation, and 50% of control fibroblast dihydroxyacetone phosphate acyltransferase activity. An increase in erythrocyte plasmalogen levels following therapy was clearly demonstrated in the milder patient, and neither patient showed evidence of toxicity. Evaluation of therapy by comparison to the usual clinical course of Zellweger syndrome was not helpful because of the variability and incomplete documentation of 90 previously reported cases. The literature survey did provide criteria for classic Zellweger syndrome, which include hypotonia with or without deformation of limbs, large fontanels and split sutures, prominent forehead, flattened facial profile with hypoplastic supraorbital ridges, anteverted nares, highly arched palate, cryptorchidism or labial hypoplasia, hepatomegaly or elevated liver enzymes, peripheral pigmentation of the retina, renal cortical cysts, and characteristic neuropathology involving decreased myelinization, abnormal neuronal migration, and sudanophilic macrophages. Less severe patients, as exemplified by our case 2 and others from the literature, will not have all the classic features and can be recognized only by a growing panel of biochemical indicators. Our patient studies illustrate the complexity of designing comprehensive therapy for Zellweger-like conditions, suggest other diseases that may involve peroxisomal alterations, and emphasize the need for multicenter, collaborative studies to evaluate biochemical heterogeneity and therapy of peroxisomal disorders.

Adrenoleukodystrophy↗
PubMed1993

Tipping of flagellar agglutinins by gametes of Chlamydomonas reinhardtii.

The migration of cross-linked agglutinins to the gametic flagellar tips (tipping) is a hallmark of the Chlamydomonas mating reaction. In this study, an assay was developed to analyze the kinetics and biological requirements for the tipping response: isolated flagella from mt- gametes of C. reinhardtii were allowed to agglutinate to the immotile flagella of pf-18 mt+ gametes, and their migration to the tips was monitored by phase microscopy. The tipping process is shown to require both adhesion and elevated levels of cAMP. The cAMP may activate tipping motors directly. In addition, cAMP stimulates the recruitment of agglutinins to the flagellar surface to replace those inactivated by adhesion. These results are compared with previous studies on the tipping of flagellar surface proteins cross-linked by soluble ligands, and an integrated model is presented.

1-Methyl-3-isobutylxanthine↗
PubMed2005

Nanoscale imaging and quantification of local proteolytic activity.

Proteolytic cleavage of extracellular matrix (ECM) is a critical feature of tumor cell invasion, and affects cancer cell growth, differentiation, apoptosis, and migration. Malignant cells secrete most proteases as inactive proenzymes that undergo proteolytic cleavage for activation, and proteolytic activity is elevated in close proximity to these cells. Therefore, local activity rather than protease concentration determines ECM proteolysis. Precise quantification of local proteolytic activity, functional investigation, and high resolution imaging of morphological ECM alterations have proven difficult. In this study, we present a novel approach for measuring proteolytic activity in the microenvironment of cells by using atomic force microscopy (AFM). Amelanotic melanoma cells (A7-clone) were seeded on fluorescent gelatin or collagen-IV coatings. Proteolysis reduced fluorescence of these coatings. Fluorescence microscopy (FM) in combination with AFM was used to maneuver the AFM-tip to tumor cell induced proteolytic spots. AFM enabled nanoscale volume measurement, three-dimensional reconstruction of single proteins and demonstrated that ECM cleavage is restricted to the proteolytic microenvironment of cancer cells. This method detected significant decreases in molecular weight of protein clusters (-76.6%), matrix volume (-46.6%), and height (-38.1%) between intact and proteolyzed gelatin. Similar parameter changes were demonstrated without FM, by AFM-scanning gelatin in close proximity to invasive cells. Furthermore, AFM depicted significantly stronger local degradation of gelatin than collagen-IV by A7-cells. Taken together, AFM allows specific quantification and imaging of local proteolytic processes at a nanometer level, thus providing a unique method for the functional evaluation of invasiveness and metastatic potential of tumor cells in small scale samples.

Animals↗
PubMed1995

Involvement of cyanide-resistant respiration in cell-type proportioning during Dictyostelium development.

Involvement of cyanide (CN)-resistant respiration in cell-type proportioning was analyzed using the developmental system of Dictyostelium discoideum. When migrating slugs were vitally stained with rhodamine 123, which is known to stain actively respirating mitochondria coupled with an elevated electronic potential of the inner membrane, the posterior prespore region was stained more strongly than the anterior prestalk region. Application of benzohydroxamic acid (BHAM) and propyl gallate, specific inhibitors of CN-resistant respiration, to starved Dictyostelium cells induced formation of unique cell masses, in which almost all of the cells differentiated into stalk-like cells with a large vacuole and thick cell wall. BHAM was also found to enhance the expressions of prestalk-specific genes such as ecmA and ecmB in the unique cell mass in a position-dependent manner. In contrast, the expression of a prespore-specific gene, Dp87, was almost completely inhibited by BHAM. Taken together these results strongly suggest the involvement of CN-resistant respiration in the proportion regulation of cell types differentiating during the Dictyostelium development.

Animals↗
PubMed1998

Coordinated actions of RuvABC in Holliday junction processing.

The RuvA, RuvB and RuvC proteins of Escherichia coli process Holliday junctions during genetic recombination and DNA repair. Biochemical studies have shown that RuvA and RuvB promote branch migration whereas RuvC resolves junctions by endonucleolytic cleavage. Here we show that RuvAB stimulate Holliday junction resolution by RuvC. Elevated RuvC activity was dependent upon RuvAB-mediated ATP-hydrolysis. These results show that the three Ruv proteins work in a coordinated manner to promote Holliday junction resolution, and account for the resolvase-defective phenotype exhibited by ruvA, ruvB or ruvC mutant strains.

Adenosine Triphosphate↗
PubMed1995

Inferior rectal nerve stimulation for anal sphincteric control: experimental study.

The effect of inferior rectal nerve (IRN) stimulation on sphincteric control of the rectal neck was studied in eight dogs. With the dog under anesthesia, the IRN was exposed through para-anal incision, and a bipolar electrode was applied to it. Response of the rectal and rectal neck pressures as well as external and sphincter (EAS) EMG activity to IRN stimulation was determined. IRN stimulation resulted in increase in both the rectal neck pressure (P < 0.01) and the EMG activity of EAS (P < 0.01). Response increased with increasing stimulation frequency up to 50 Hz, above which no more response occurred. Rectal pressure showed no change (P > 0.05). Both the latency and the duration of response decreased with increased stimulation. The response was resumed after an off-time of twice the stimulation phase. Long-term activation has not been associated with an impairment of nerve responsiveness or with electrode migration or break. To conclude, a stimulus of 50 Hz evokes the most adequate EAS contraction and RN pressure elevation. Chronic electrostimulation of the perineal nerve may restore EAS tone.

Action Potentials↗
PubMed1992

Use of a reconstituted basement membrane to study the invasiveness of tumor cells.

We have used an extract of basement membranes which can be reconstituted into a biologically active gel matrix composed predominantly of collagen IV, laminin, nidogen, and heparin sulfate proteoglycan, in order to study the mechanisms involved in tumor cell invasion. When layered onto a porous filter in a Boyden chamber, the gel forms a barrier to the passage of normal cells. Malignant cells are able to cross this layer when the conditioned medium of NIH 3T3 cells is used as a chemoattractant to stimulate cell migration. A variety of human tumor cells have thus been studied in this system and we find a high correlation between their invasiveness in vitro and their malignant behavior as exhibited in vivo. We have used this in vitro invasion assay to test for factors which might inhibit tumor cell invasion. Collagenase IV is produced by malignant cells and is thought to be required for invasion. Indeed, inhibitors of this enzyme have demonstrated reduced tumor cell invasiveness. One site of five amino acids, on the B1 chain, which has been shown to promote cell adhesion, migration and binding to laminin receptor, was found to inhibit the invasion of tumor cells. In addition, factors which elevated cAMP levels were also able to suppress the invasiveness of tumor cells. These data suggest that the assay system described herein can be successfully utilized to study the invasive activity of tumor cells and those factors that may inhibit the spread of malignant cells.

1-Methyl-3-isobutylxanthine↗
PubMed1996

The distribution and partial characterization of FMRFamide-related peptides in the salivary glands of the locust, Locusta migratoria.

The distribution and partial characterization of FMRFamide-related peptides in the salivary glands of the locust, Locusta migratoria, were investigated by means of immunohistochemistry, radioimmunoassay and reversed-phase high performance liquid chromatography. Whole-mount preparations of glands stained positively against anti-FMRFamide antisera, and contained the equivalent of 837 +/- 80 fmol FMRFamide/gland pair, as determined by radioimmunoassay. FMRFamide-like immunoreactivity occurred in the processes of the transverse nerves of both the prothoracic and mesothoracic ganglia, but was not found in the salivary motoneurons 1 or 2 of the suboesophageal ganglion, both of which directly innervate the salivary glands via the salivary nerve 7b; nor was it found within the salivary nerve 7b itself, leading to the salivary glands. It was, however, found as a superficial nerve plexus on the surface of nerve 7 at the suboesophageal ganglion, but did not appear to extend to the salivary glands. The origin of this staining is unclear. High performance liquid chromatography of salivary gland tissue extracts, monitored by radioimmunoassay, revealed 4 peaks of immunoreactive material, 2 of which co-migrated with AFIRFamide and GQERNFLRFamide, previously isolated from the locust ventral nerve cord. These 2 synthetic peptides did not elevate basal levels of the second messengers cyclic AMP or cyclic GMP in the salivary glands.

Amino Acid Sequence↗
PubMed1983

Calcium-dependent association of glutathione S-transferase with the human erythrocyte membrane.

Elevations in intracellular calcium increase the adsorption of a cytoplasmic protein to human red blood cell membrane. This protein migrates on SDS polyacrylamide gels at 23,000 daltons and has been called band 8. The association of this protein with the membrane is increased in sickle cell anemia. This protein is extracted from the membrane with EGTA, a calcium chelator. Enzymatic and immunological studies identify band 8 as a glutathione S-transferase.

Anemia, Sickle Cell↗