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PubMed2001

Discrimination between peak spreading in capillary zone electrophoresis of proteins due to interaction with the capillary wall and due to protein microheterogeneity.

Our study attempts to find an approach to distinguishing between the contribution to peak spreading in capillary zone electrophoresis (CZE) due to protein microheterogeneity and that due to interaction with the capillary wall, by analyzing correlations between observed peak spreading and peak asymmetry. The peak asymmetry was measured as ln[(tm-t1)/(t2-tm)] where tm, t1, and t2 are migration times at the mode of the peak and at the intersection of the peak width at half-height with the ascending and descending limbs, respectively. Two isoforms of recombinant green fluorescent protein (GFP-1 and GFP-2, 27 kDa molecular mass), glucose-6-phosphate dehydrogenase (GPD, 104 kDa), and the naturally fluorescent protein R-phycoerythrin (PHYCO, 240 kDa) were subjected to CZE in polyacrylamide-coated fused-silica capillaries of 50 and 100 microns diameters under varying conditions of protein concentration, field strength, and the initial zone length. Under conditions such that contributions to peak spreading from axial diffusion, thermal effects, and electrophoretic dispersion are negligible, the analysis of the interrelations between peak width and peak asymmetry was found to allow a conclusion as to the cause of peak spreading in CZE of protein. It appears that the peak width of GFP-2 originates mostly in protein microheterogeneity while that of GFP-1 is due to protein-capillary wall interactions. For PHYCO, both microheterogeneity and protein-capillary wall interactions contribute to peak spreading. GPD exhibits relatively little microheterogeneity or interaction with capillary walls. Thus, its peak width appears to be mostly affected by an extracolumn source of spreading such as the initial zone length.

Electrophoresis, Capillary↗

PubMed2002

Squamous cell carcinoma of the upper aerodigestive tract: the prevalence of microscopic extracapsular spread and soft tissue deposits in the clinically N0 neck.

BACKGROUND: With squamous cell carcinoma of the upper aerodigestive tract the presence or absence of neck metastases is the most important prognostic factor. This makes the histopathologic assessment of neck dissections of paramount importance. With the clinically N0 neck the prevalence of microscopic extracapsular spread and soft tissue deposits has not previously been described. METHODS: We have prospectively analyzed 96 elective neck dissections in 63 patients with upper aerodigestive tract squamous cell carcinoma and clinically N0 necks to assess the prevalence of microscopic extracapsular spread and soft tissue deposits. The dissections were separated peroperatively into nodal levels; these were sectioned at 6-microm sections and stained with H & E. RESULTS: Nineteen patients (30.2%) were upstaged to pN+ve. Twelve of these had microscopic extracapsular spread, which was 19.0% of the clinically N0 necks and 63.2% of the pN+ve. Five had soft tissue deposits, which was 7.9% of the clinically N0 necks. Fourteen patients had microscopic extracapsular spread and/or soft tissue deposits, which represented 22.2% of all necks examined and 73.7% of the pN+ve necks. CONCLUSIONS: Microscopic extracapsular spread and soft tissue deposits have a high prevalence in patients with clinically N0 necks. Extracapsular spread can occur at an early stage in metastasis from upper aerodigestive tract squamous cell carcinoma. Soft tissue deposits can also occur at an early stage. Soft tissue deposits may occur by the same process as lymph node metastasis with total effacement of the lymph node or may occur by some other process such as lymphatic tumor embolization.

Carcinoma, Squamous Cell↗

PubMed2003

Cervical node metastases in squamous cell carcinoma of the upper aerodigestive tract: the significance of extracapsular spread and soft tissue deposits.

BACKGROUND: Literature regarding the prognostic significance of extracapsular spread and soft tissue deposits in cervical lymph node metastases of squamous cell carcinoma of the upper aerodigestive tract shows variable results. METHODS: We analyzed 215 prospectively collected neck dissections from 155 patients with upper aerodigestive tract squamous cell carcinoma to assess the prevalence of extracapsular spread and soft tissue deposits and to assess their effect on survival. RESULTS: Both extracapsular spread and soft tissue deposits significantly reduced survival (actuarial and recurrence free) compared with pN0 necks (p <.001) and pN+ve necks without extracapsular spread (p <.0025). There was no statistically significant difference between pN+ve necks without soft tissue deposits or extracapsular spread compared with those with pN0 necks (p =.24). Multivariate analysis revealed comparable results. CONCLUSIONS: Microscopic and macroscopic extracapsular spread and soft tissue deposits are of prognostic significance for survival and recurrence-free survival in patients with upper aerodigestive tract squamous cell carcinoma.

Carcinoma, Squamous Cell↗

PubMedDate not supplied

Patterns of spread of squamous cell carcinoma to the ramus of the mandible.

Patterns of spread of squamous cell carcinoma to the ramus of the mandible have been studied. In nonirradiated mandibles, tumor in the ramus was found to have spread in continuity from tumor within the body. In 22 of 27 specimens (81.5%) with established invasion of the molar region of the body, tumor spread was either confirmed to the body or to the body and the anterior part of the ramus. The remaining five cases showed extensive spread within the ramus. It was concluded that a more conservative approach to resection of the ramus may be safe on pathologic grounds in the nonirradiated mandible. In postirradiation mandibles, direct invasion through cortical bone was seen in addition to direct spread from the body. Tumor spread to the ramus was seen in nine of 12 specimens (75%), and in each case was both diffuse and extensive. It was concluded that a conservative approach to resection of the ramus is not safe on pathologic grounds after radiotherapy.

Carcinoma, Squamous Cell↗

PubMed1983

Interaction of fibroblasts and polymer surfaces: relationship between surface free energy and fibroblast spreading.

Cell spreading and cell division rates of a transformed line of mouse lung fibroblasts were studied on various polymer surfaces in the presence of serum proteins. The bare polymer surfaces, as well as the protein-coated surfaces, were characterized by their polar (gamma ps) and dispersion (gamma ds) surface free energies. Cell spreading appeared to be dependent on the polar surface free energy. Cell spreading is low when the gamma ps of the bare surface is lower than 5 erg cm-2; marked spreading occurs when gamma ps is higher than 15 erg cm-2. A similar relationship was found between cell spreading and polarity of the protein-coated surfaces, although less pronounced than for the bare surfaces. Cell spreading appeared independent of the dispersion surface free energy. Cell division rate was the same on all surfaces tested.

Animals↗

PubMed2002

Insulin stimulates spreading of skeletal muscle cells involving the activation of focal adhesion kinase, phosphatidylinositol 3-kinase and extracellular signal regulated kinases.

Insulin plays an important role in muscle cell survival and proliferation. However, there is no report showing the role of insulin in spreading of muscle cells. In the present report, we showed that insulin enhances muscle cell spreading concomitant with enhanced tyrosine phosphorylation of focal adhesion kinase (FAK) and paxillin. Moreover, insulin can stimulate the cell spreading even in presence of integrin alpha5 blockers although to a lesser extent as compared to control. Cell adhesion was not dependent on insulin and serum, and decreased in presence of integrin blockers. We found direct association of FAK with affinity purified insulin receptors using in vitro kinase assay. The increase in FAK tyrosine phosphorylation was associated with increase in its kinase activity and further supported by increased phosphotyrosine accumulation on focal adhesions and increased membrane localization of FAK after stimulation by insulin. Moreover, insulin-mediated muscle cell spreading was dependent upon phosphatidylinositol 3-kinase (PI 3-kinase) activity. PI 3-kinase activity was found to be associated with FAK and the FAK associated PI 3-kinase activity enhanced when cells were plated in presence of insulin. We also observed activation of MAP kinases, i.e., ERK-1/-2 during insulin mediated muscle cell spreading. In conclusion, FAK, PI 3-kinase, and MAP kinase are important components of pathway(s) that regulate insulin stimulated muscle cell spreading.

Androstadienes↗

PubMed1975

Cell to substrate adhesion and spreading: inhibition by cationic anesthetics.

The plasma membrane is the postulated site of action of anesthetics on nerve or muscle. The drugs may be useful in the analysis of membrane phenomena in other cells. We show here that cationic anesthetics and tranquilizers inhibit cell adhesion and spreading, metabolically dependent processes that involve membrane motility and changes in cell shape. Adhesion was measured by layering 51Cr labeled Sarcoma I (Sa I) cells on glass coverslips for 20 minutes at 34 degrees C, rinsing and estimating the glass-associated radioactivity. Spreading was evaluated microscopically. Both cell adhesion to untreated glass and the Mn2+ dependent adhesion to serum-coated coverslips were inhibited by the drugs, in the following order of increasing activity: tetracaine, promethazine, cyclomethycaine, chlorpromazine and fluphenazine. Similar ranks of drug activity have been reported for nerve blocking, inhibition of cell fusion and inhibition of induced spreading of macrophages. Microscopic observations showed the drugs also inhibited MN2+ INDUCED SPREADING OF Sa I. Drug treated cells were rounded, refractile, devoid of cell processes or ruffles visible by light microscopy. The effects of the drugs on adhesion and spreading were reversible upon washing of the cells. We postulate that the inhibition of adhesion and spreading are a consequence of the inhibition of cell surface motility by the anesthetics.

Anesthetics, Local↗

PubMed1980

Spreading of human fibroblasts in serum-free medium: inhibition by dithiothreitol and the effect of cold insoluble globulin (plasma fibronectin).

We have tested the effect of dithiothreitol (DTT) treatment on the initial spreading of human fibroblasts in serum-free medium in tissue culture dishes. Cell spreading was inhibited following treatment of these cells with 10 mM DTT. Inhibition occurred when the cells were treated at 37 degrees C but not at 4 degrees and was reversible metabolically but not by the addition of sulfhydryl oxidizing reagents. The inhibition was overcome when DTT-treated human fibroblasts were plated on cold insoluble globulin (plasma fibronectin)--coated dishes. Under these conditions spreading appeared to be completely normal, including the formation of focal adhesions. Analysis of the fibronectin concentrations in the human fibroblasts following DTT treatment indicated that there was little decrease in the absolute level of activity as determined in a biological assay for BHK cells spreading on culture dishes. Analysis of the fibronectin distribution on the DTT-treated human fibroblasts by indirect immunofluorescence using a specific anti-CIG antiserum revealed that fibronectin was no longer deposited onto the culture dish surfaces. Even when the DTT-treated human fibroblasts spread in the presence of fetal calf serum, the cell fibronectin remained for the most part in a perinuclear location. These results indicate that DTT treatment of human fibroblasts prevents the normal translocation of fibronectin from a perinulear location to the surface of the culture dish. This study further supports our hypothesis that the initial spreading in serum-free medium of fibroblasts from cell strains depends upon secretion of fibronectin onto the culture dish surface.

Animals↗

PubMed1984

Fibroblast spreading and phagocytosis: similar cell responses to different-sized substrata.

Experiments were carried out to test the hypothesis that cell spreading and phagocytosis are similar cell responses to different-sized substrata. The following morphological and biochemical studies provided evidence for this supposition. Cells phagocytosed 1.09-micron and 5.7-micron latex beads, but were unable to completely ingest 15.8-micron or 25.7-micron beads. With the larger beads, the cells spread around the bead surfaces with an appearance typical of cells spread on culture dishes. Biochemical studies with cytochalasin D, azide, and iodoacetate, as well as temperature-dependence studies, demonstrated similar responses of cell spreading and phagocytosis to these treatments. Similar cell surface receptors were involved in cell spreading and phagocytosis based upon experiments using antibodies to baby hamster kidney (BHK) cell wheat germ agglutinin receptors. And finally, BHK cell variants with defective plasma fibronectin (pFN) receptors were unable to spread on pFN-coated dishes or ingest pFN-coated beads. Evidence also is presented concerning the "contact" process in cell adhesion. It was found that azide and low temperature inhibited cell attachment per se but did not block fibronectin-receptor interactions based upon cell binding of pFN-coated beads. A possible explanation for the contact process is presented based upon the resistance of cells and beads to shear forces.

Animals↗

PubMed1988

Concanavalin A-induced impairment of fibroblast spreading on laminin but not on fibronectin.

The effect of concanavalin A (Con A) on the adhesion of 8-day-old chick embryo fibroblasts (CEFs) to fibronectin (FN) and laminin (LM) was studied. Con A was shown to inhibit the spreading of CEF on a LM substrate. In contrast, no inhibition of CEF spreading on the FN substrate could be detected when the quantity of FN coated varied from 0.5 to 4 pmoles. The effect induced by Con A was specific, since it was abolished by 100 mM alpha-methylmannopyranoside. The inhibition of CEF spreading was only observed when the lectin was added during the 20 min following cell plating. In addition, the effect of Con A on CEF spreading on the LM substrate was shown to be dependent upon its presence at the cell surface, since under conditions which accelerate the uptake of the lectin, the effect on cell spreading is no longer detectable. Furthermore, the number of CEFs attached to LM was not modified by the lectin. The molecular weight of the isolated Con A binding sites revealed glycoproteins ranging from 30,000 to 72,000. On the other hand, these Con A binding sites did not interact with LM-Sepharose. Only a protein with a molecular weight of 68,000 which did not express affinity for Con A bound tightly to the LM-Sepharose. These data suggested that cell surface Con A binding sites do not interfere with the initial step of CEF adhesion to LM but play a key role during their spreading on this glycoprotein.

Animals↗

PubMed2006

The C-terminal Ca2+-binding domain of SPARC confers anti-spreading activity to human urothelial cells.

The anti-spreading activity of secreted protein acidic and rich in cysteine (SPARC) has been assigned to the C-terminal third domain, a region rich in alpha-helices. This "extracellular calcium-binding" (EC) domain contains two EF-hands that each coordinates one Ca2+ ion, forming a helix-loop-helix structure that not only drives the conformation of the protein but is also necessary for biological activity. Recombinant (r) EC, expressed in E. coli, was fused at the C-terminus to a His hexamer and isolated under denaturing conditions by nickel-chelate affinity chromatography. rEC-His was renatured by procedures that simultaneously (i) removed denaturing conditions, (ii) catalyzed disulfide bond isomerization, and (iii) initiated Ca2+-dependent refolding. Intrinsic tryptophan fluorescence and circular dichroism spectroscopies demonstrated that rEC-His exhibited a Ca2+-dependent conformation that was consistent with the known crystal structure. Spreading assays confirmed that rEC-His was biologically active through its ability to inhibit the spreading of freshly plated human urothelial cells propagated from transitional epithelium. rEC-His and rSPARC-His exhibited highly similar anti-spreading activities when measured as a function of concentration or time. In contrast to the wild-type and EC recombinant proteins, rSPARC(E268F)-His, a point substitution mutant at the Z position of EF-hand 2, failed to exhibit both Ca2+-dependent changes in alpha-helical secondary structure and anti-spreading activity. The collective data provide evidence that the motif of SPARC responsible for anti-spreading activity was dependent on the coordination of Ca2+ by a Glu residue at the Z position of EF-hand 2 and provide insights into how adhesive forces are balanced within the extracellular matrix of urothelial cells. .

Adolescent↗

PubMed1980

Effects of a serum spreading factor on growth and morphology of cells in serum-free medium.

A heat-sensitive, trypsin-sensitive factor that promoted growth and spreading of cells in serum-free, hormone-supplemented medium was partially purified from human serum. The major portion of the proteins in these preparations migrated upon SDS-polyacrylamide gel electrophoresis with a mobility consistent with molecular weights between 60,000 and 90,000. The spreading activity, which we have termed serum spreading factor, stimulated growth and spreading of a wide variety of cell types. The serum spreading factor was similar to fibronectin in that it showed an affinity for the plastic cell culture substrate but was shown to be distinct from fibronectin by several criteria. This factor may prove useful in studies of cell attachment and spreading and in studies of the relationship of cell shape and cell proliferation.

Animals↗

PubMed1997

Measurement of the point spread function in MRI using constant time imaging.

The point spread function is a fundamental property of magnetic resonance imaging methods that affects image quality and spatial resolution. The point spread function is difficult to measure precisely in magnetic resonance even with the use of carefully designed phantoms, and it is difficult to calculate this function for complex sequences such as echo-planar imaging. This report describes a method that measures the point spread function with high spatial resolution at each pixel in samples of uniform intensity distribution. This method uses additional phase encoding gradients before the echo-planar acquisition that are constant in length but vary in amplitude. The additional gradients are applied to image the contents within each individual voxel. This method has been used to measure the point spread function for echo-planar imaging to demonstrate the effects of limited k-space sampling and transverse relaxation, as well as the effects of object motion. By considering the displacement of the point spread function, local distortions due to susceptibility and chemical shift effects have been quantified and corrected. The method allows rapid assessment of the point spread function in echo-planar imaging, in vivo, and may also be applied to other rapid imaging sequences that can be modified to include these additional phase encoding gradients.

Brain↗

PubMed1994

The influences of attitudes, beliefs and label information on perceptions of reduced-fat spread.

A sample of 101 consumers completed questionnaires assessing use, attitudes and beliefs with regard to full- and reduced-fat (FF and RF) spreads. In sensory tests, they rated liking of selected attributes and overall liking of a RF spread sample labelled as "reduced-fat spread 40% fat" or "full-fat margarine 80% fat". The amount spread onto bread was also determined. Other than an effect on likelihood of consumption, there were no consistent effects of label alone on any of these measures. However, analyses of sensory and hedonic ratings revealed consistent interactive effects of label information with consumer attitudes, beliefs, and (to a lesser degree) with the type of spread normally used. Eating restraint and body composition were generally unrelated to sensory ratings and response to label information. The overall effect of label information was to shift sensory judgments in a direction more consistent with an individual's beliefs; i.e., hedonic responses from subjects with more positive attitudes toward RF or FF spreads were significantly greater in the respective label condition. Given this potential differential influence of labelling, we recommend that consumer trials manipulating provision of information should include measures assessing subjects' attitudinal characteristics.

Adolescent↗

PubMed1999

Ca(2+)-independent phospholipase A2 is required for alpha2-adrenergic-induced preadipocyte spreading.

In the present study, we studied the involvement of A2 phospholipases (PLA2) in alpha2-adrenergic receptor-control of preadipocyte actin cytoskeleton. For that, various PLA2 inhibitors were tested on the ability of the selective alpha2-adrenergic agonist UK14304 to induce the spreading in alpha2AF2 preadipocytes. We observed that, whereas several Ca(2+)-dependent PLA2 blockers were ineffective, the Ca(2+)-independent phospholipase A2 (iPLA2) inhibitor, broenolactone (BEL), specifically blocked alpha2-adrenergic-dependent preadipocyte spreading without affecting the spreading activity of lysophosphatidic acid (LPA) or serum. BEL inhibition was completely restored by lysophosphatidic acid, but not by arachidonic acid or other fatty acids. The presence of the lysophospholipase (phospholipase B) suppressed the effect of LPA on preadipocyte spreading, but had no influence on alpha2-adrenergic-induced spreading. Thus, the extracellular production of LPA or fatty acids is not involved in iPLA2-dependent preadipocyte spreading. iPLA2 protein was found in preadipocytes but, conversely to cPLA2, did not exhibit any modification of its electrophoretic mobility after alpha2-adrenergic stimulation. We concluded that iPLA2 is involved in alpha2-adrenergic control of preadipocyte actin cytoskeleton.

3T3 Cells↗

PubMed2000

HGF/SF-induced spreading of MDCK cells correlates with disappearance of barmotin/7H6, a tight junction-associated protein, from the cell membrane.

Changes in expression of the two tight junction-associated proteins, barmotin/7H6 and ZO-1, as well as the adherence junction-associated protein, E-cadherin, were followed during hepatocyte growth factor/scatter factor (HGF/SC)-induced migration process of MDCK cells. Modulation of the HGF/SF-induced migration process by staurosporine, an inhibitor of protein kinase C (PKC), was also examined. Cell migration induced by HGF/SF consisted of two distinct phases, initial cell spreading between 2 and 9 h after the start of treatment, and the scattering phase which started approximately 12 h after treatment. Both ZO-1 and E-cadherin were expressed at the cell-cell border of adherent cells in the scattering phase, whereas barmotin/7H6, a barrier function-related tight junction protein, was not seen during the early spreading phase. Confluent cultures of MDCK cells, which did not spread after HGF/SF treatment, were positive for barmotin/7H6 expression at cell-cell borders. Blocking PKC activation during HGF/SF treatment with staurosporine inhibited cell spreading, and the cells retained barmotin/7H6 expression until at 6 h after HGF/SF treatment. The results indicate that disappearance of the tight junction protein, barmotin/7H6, is closely associated with cell spreading, with both barmotin/7H6 expression and cell spreading seemingly being regulated by PKC-mediated signaling.

Animals↗

PubMed1998

Function and expression of CD44 during spreading, migration, and invasion of murine carcinoma cells.

The cell surface glycoprotein CD44 is proposed as a main participant in cell adhesion and migration. We studied the function, expression, and distribution of CD44 in the invasive and metastatic F3II murine carcinoma cell line during adhesion, spreading, migration, and invasion. A mAb anti-CD44 (KM 201) dramatically blocked F3II cell adhesion on both plastic and hyaluronic acid coatings, as well as spreading on uncoated plastic surfaces (P < 0.01). KM201 mAb significantly inhibited F3II cell migration and invasion in Transwell chambers. Immunocytochemistry of spreading cells revealed that CD44 distributed in bands on the cell surface, particularly in the tip of leading edges and in the perinuclear zones of the cell membrane. CD44 antigen was never detected in filopodia or lamellipodia nor in focal adhesion-like structures, but was also detectable as strong interlamellar bands. Fully spread cells showed a decreased CD44 signal compared to cells in early stages of spreading. This decrease correlated with a reduced expression of CD44 as detected by Western blot. We also investigated the signals that may regulate CD44 expression in F3II cells. Treatment of F3II cells, with phorbol myristate acetate (PMA) or phosphatidic acid (PA, the product of PLD-dependent hydrolysis of phosphatidylcholine), significantly enhanced CD44 expression. Conversely, the treatment of F3II cells with H7, a specific PKC inhibitor, or propranolol, which blocks PA conversion to DAG, significantly decreased CD44 expression levels. These results suggest the involvement of PKC and PLD pathways in CD44 expression. These results demonstrate that CD44 plays an important role during F3II cells adhesion, spreading, migration, and invasion. In addition we provide information linking the PLD- and PKC-dependent pathways with the regulation of CD44 expression.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1997

Effects of coat protein mutations and reduced movement protein expression on infection spread by cowpea chlorotic mottle virus and its hybrid derivatives.

Previously we have reported that the essential 3a movement gene of icosahedral cowpea chlorotic mottle virus (CCMV) can be functionally replaced by the 30-kDa movement gene of rod-shaped sunn-hemp mosaic virus (SHMV). Because plant RNA viruses differ in requiring or not requiring coat protein for systemic infection, we have now investigated whether systemic spread by this CCMV/SHMV hybrid is dependent on its CCMV coat protein as well as its SHMV movement protein. We find that either deletion or frameshift mutations in the coat protein gene block systemic spread. Thus, like wild-type CCMV, systemic infection by the hybrid is dependent on both movement protein and coat protein. These results further support the conclusion that the required functions of the coat and movement proteins in CCMV spread do not depend on sequence-specific interaction between these proteins. Additional features of the hybrid also motivated testing the effects of modulating movement protein expression. Creating an extra, out-of-frame translational start codon (AUG) shortly upstream of the 3a movement protein gene in CCMV downregulated its expression 18-fold. Nevertheless, for CCMV derivatives bearing either the CCMV 3a gene or the SHMV 30-kDa gene, the extra AUG resulted in only a minor delay in the onset of viral spread and little or no effect on the subsequent rate of cell-to-cell spread. Thus, under normal circumstances, the rate of CCMV cell-to-cell spread in cowpea plants appears to be limited primarily by factors other than movement protein synthesis.

Amino Acid Sequence↗