Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spreading”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,495 records · Page 83Linked to original sources
PubMed2005

Quantitative measurement of changes in adhesion force involving focal adhesion kinase during cell attachment, spread, and migration.

Focal adhesion kinase (FAK) is a critical protein for the regulation of integrin-mediated cellular functions and it can enhance cell motility in Madin-Darby canine kidney (MDCK) cells by hepatocyte growth factor (HGF) induction. We utilized optical trapping and cytodetachment techniques to measure the adhesion force between pico-Newton and nano-Newton (nN) for quantitatively investigating the effects of FAK on adhesion force during initial binding (5 s), beginning of spreading (30 min), spreadout (12 h), and migration (induced by HGF) in MDCK cells with overexpressed FAK (FAK-WT), FAK-related non-kinase (FRNK), as well as normal control cells. Optical tweezers was used to measure the initial binding force between a trapped cell and glass coverslide or between a trapped bead and a seeded cell. In cytodetachment, the commercial atomic force microscope probe with an appropriate spring constant was used as a cyto-detacher to evaluate the change of adhesion force between different FAK expression levels of cells in spreading, spreadout, and migrating status. The results demonstrated that FAK-WT significantly increased the adhesion forces as compared to FRNK cells throughout all the different stages of cell adhesion. For cells in HGF-induced migration, the adhesion force decreased to almost the same level (approximately 600 nN) regardless of FAK levels indicating that FAK facilitates cells to undergo migration by reducing the adhesion force. Our results suggest FAK plays a role of enhancing cell adhesive ability in the binding and spreading, but an appropriate level of adhesion force is required for HGF-induced cell migration.

Animals↗
PubMed2005

ADAM22 plays an important role in cell adhesion and spreading with the assistance of 14-3-3.

Cellular adhesion plays important roles in a variety of biological processes. The ADAM family contains disintegrin-like and metalloproteinase-like domains which potentially have cell adhesion and protease activities. Recent studies suggest that the interaction between 14-3-3zeta and ADAM22cyt can regulate cell adhesion and spreading, therefore it has a potential role in neural development and function. 14-3-3 family has seven highly conserved members that regulate various cellular functions. Using yeast two-hybrid method, we identified that ADAM22cyt bound some other 14-3-3 family members. The interaction was further confirmed by in vitro protein pull-down assay and co-immunoprecipitation. We also found that the overexpression of exogenous ADAM22 in HEK293 cells could significantly enhance cell adhesion and spreading, compared with the truncated ADAM22 lack of 14-3-3 binding motifs. These results strongly demonstrated a functional role for ADAM22/14-3-3 in cell adhesion and spreading.

14-3-3 Proteins↗
PubMed2004

Hepatocyte behavior on synthetic glycopolymer matrix: inhibitory effect of receptor-ligand binding on hepatocyte spreading.

The interaction of carbohydrate-based polymers with asialoglycoprotein receptors (ASGPRs) on the surface of hepatocytes has been used to design hepatocyte adhesion matrices. Therefore, we have characterized the interaction of ASGPR on the surface of hepatocytes with glycopolymer-coated surfaces. Since ASGPRs bound to glycopolymer surfaces escape from internalization and degradation, they were quantified by western blot analysis. The amount of hepatocyte ASGPRs that initially adhered to the glycopolymer surface was proportional to the concentration of the coated glycopolymer. We found that the initial adhesion of hepatocytes to the glycopolymer surface was enhanced by interactions with ASGPR, whereas interactions with ASGPR inhibited the post-adhesion process, a cell adhesion phenomenon that occurs following the initial adhesion. Furthermore, hepatocytes are much more spread on glycopolymer surfaces with lower coating density. Taken together, we suggest that the post-adhesion process triggered hepatocyte spreading on glycopolymer surfaces, and ASGPR-carbohydrate interactions act negatively on the post-adhesion mechanism as well as on hepatocyte spreading on glycopolymer surfaces depending on the density of coated glycopolymers.

Animals↗
PubMed2006

Combinatorial screen of the effect of surface energy on fibronectin-mediated osteoblast adhesion, spreading and proliferation.

In order to accelerate tissue-engineering research, a combinatorial approach for investigating the effect of surface energy on cell response has been developed. Surface energy is a fundamental material property that can influence cell behavior. Gradients in surface energy were created by using an automated stage to decelerate a glass slide coated with a self-assembled monolayer (SAM, n-octyldimethylchlorosilane) beneath a UV lamp such that the SAM is exposed to the UV-light in a graded fashion. UV exposure causes oxidation of the SAM such that a longer exposure correlates with increased hydrophilicity. This approach yielded substrates having a linear gradient in surface energy ranging from 23 to 62 mN/m (water contact angles ranging from 25 degrees to 95 degrees ). Using the gradient specimen approach enables all surface energies from 23 to 60 mN/m to be screened on each slide. Before cell culture, surface energy gradients were coated with fibronectin to allow a study of the effect of surface energy on fibronectin-mediated cell response. Cells were seeded on the fibronectin-coated gradients and adhesion, spreading and proliferation were assessed with automated fluorescence microscopy. Surface energy did not affect initial cell adhesion at 8h. However, the rate of proliferation was linearly dependent on surface energy and increased with increasing hydrophobicity. Cell spread area was unaffected by changes in surface energy over the majority of the gradient although cells were significantly smaller on the most hydrophilic region. These results show that fibronectin-mediated cell spreading and proliferation are dependent on surface energy and establish a new combinatorial approach for screening cell response to changes in surface energy.

3T3 Cells↗
PubMed2004

Modelling the social dynamics of a sex industry: its implications for spread of HIV/AIDS.

A theoretical model is proposed for a community which has the structure of two classes (direct and indirect) of commercial sex workers (CSW), and two classes of sexually active male customers with different levels of sexual activity. The direct CSW's work in brothels while the indirect CSW's are based in commercial establishments such as bars, cafes, and massage parlours where sex can be bought on request and conducted elsewhere. Behaviour change and the resulting change of activity class occurs between the two classes of CSW's and two classes of males under the setting of the proliferation of human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome epidemic and the subsequent intervention programmes. In recently years, this phenomenon has been observed in several countries in Asia. Given the lower levels of condom use and higher HIV prevalence of the indirect CSW's, ascertaining the impact of this change in the structure of the sex industry on the spread of HIV is the main focus of this paper. The complete analysis of the disease-free model is given. For the full model, local analysis will be performed for the case of preferred mixing without activity class change, as well as the case with activity class change and restricted mixing. The basic reproduction number for the spread of epidemic will be derived for each case. Results of biological significance include: (i). the change of behaviour by the CSW's has a more direct effect on the spread of HIV than that of the male customers; (ii). the basic reproduction number is obtained by considering all possible infection cycles of the heterosexual transmission of HIV which indicates the importance of understanding the sexual networking in heterosexual transmission of HIV; (iii). the social dynamics of the sex industry is not just a simple 'supply and demand' mechanism driven by the demand of the customers, hence highlighting the need for further understanding of the changing structure of the sex industry. The main points of this work will be illustrated with numerical examples using the HIV data of Thailand.

Disease Transmission, Infectious↗
PubMed2005

Non-cholesterol sterols in serum, lipoproteins, and red cells in statin-treated FH subjects off and on plant stanol and sterol ester spreads.

BACKGROUND: Serum plant sterol levels are increased by consumption of statins and dietary plant sterols, and decreased by dietary plant stanols, but little is known about combination therapy of statin and plant sterols. METHODS: We measured plant sterols in serum, lipoproteins, and red cells in subjects with familial hypercholesterolemia (FH) (n=18) treated with variable doses of statins off and on plant stanol (STA) and sterol ester (STE) spreads. RESULTS: STA and STE spreads lowered LDL cholesterol approximately 15%. Plant sterols were decreased in serum, lipoproteins, and red cells by approximately 25% with STA and increased from 37% to 80% with STE, especially with high statin doses. The changes in serum were related to those in red cells. The baseline levels of serum plant sterols were negatively (r-range -0.639 to -0.935) and positively (r-range 0.526 to 0.598) correlated with the respective changes evoked by the STA and STE spreads. CONCLUSIONS: STE reduces LDL cholesterol, but increases serum, lipoprotein, and red cell plant sterol levels in statin-treated FH subjects, while all the respective values are decreased with STA. Recent predictions that elevated serum plant sterols pose an increased coronary risk suggest that increases of serum plant sterol levels should be avoided, especially in atherosclerosis-prone individuals, such as subjects with FH.

Adult↗
PubMed2006

Insulin degrading enzyme is a cellular receptor mediating varicella-zoster virus infection and cell-to-cell spread.

Varicella-zoster virus (VZV) causes chickenpox and shingles. While varicella is likely spread as cell-free virus to susceptible hosts, the virus is transmitted by cell-to-cell spread in the body and in vitro. Since VZV glycoprotein E (gE) is essential for virus infection, we postulated that gE binds to a cellular receptor. We found that insulin-degrading enzyme (IDE) interacts with gE through its extracellular domain. Downregulation of IDE by siRNA, or blocking of IDE with antibody, with soluble IDE protein extracted from liver, or with bacitracin inhibited VZV infection. Cell-to-cell spread of virus was also impaired by blocking IDE. Transfection of cell lines impaired for VZV infection with a plasmid expressing human IDE resulted in increased entry and enhanced infection with cell-free and cell-associated virus. These studies indicate that IDE is a cellular receptor for both cell-free and cell-associated VZV.

Animals↗
PubMed2006

Transformation by RAS oncogene decreases the width of substrate-spread fibroblasts but not their length.

We compared morphometric parameters of the contours of cells in four pairs of non-transformed mouse and rat lines and of the same lines transformed by oncogenes of the RAS family. As expected, the mean areas of all RAS-transformed lines were much smaller than those of their non-transformed counterparts. At the same time the average length of cell projection did not regularly decrease after transformation. These results show that transformation induced by expression of RAS oncogene selectively affect only one component of spreading, namely transversal spreading and not longitudinal spreading; these changes result in an increase of antero-posterior polarity of transformed fibroblasts.

Animals↗
PubMed2006

CpG DNA enhances macrophage cell spreading by promoting the Src-family kinase-mediated phosphorylation of paxillin.

Macrophages are an important component of the innate immune response to infection by microbial pathogens. The activation of macrophages by pathogens is largely mediated by Toll-like receptors (TLRs). Bacterial DNA, which contains unmethylated CpG dinucleotide motifs, is specifically recognised by TLR9 and triggers the activation of a complex network of intracellular signalling pathways that orchestrates the ensuing inflammatory responses of macrophages to the pathogen. Here, we have established that CpG DNA promotes reorganisation of the actin cytoskeleton and enhances cell spreading by primary mouse bone marrow macrophages. CpG DNA stimulation resulted in an approximately 70% increase in cell size. Notably, CpG DNA-induced cell spreading was dependent on the activity of Src-family kinases. Tyrosine phosphorylation of several proteins was increased in a Src-family kinase-dependent manner following CpG DNA stimulation of bone marrow macrophages, including the cytoskeletal protein paxillin. Paxillin was phosphorylated both in vitro and in vivo by the Src-family kinase Hck. Significantly, paxillin from CpG DNA-stimulated bone marrow macrophages had a greater capacity to bind the SH2 domain of the adapter protein Crk than did paxillin from unstimulated bone marrow macrophages. Furthermore, phosphorylation of paxillin by Hck created a binding site for Crk. We propose that the formation of paxillin-Crk complexes may mediate the cytoskeletal changes that underlie the increased cell spreading of macrophages following their activation by CpG DNA.

Animals↗
PubMed2006

Hydrophobic interaction chromatography of proteins IV. Kinetics of protein spreading.

Adsorption of proteins on surfaces of hydrophobic interaction chromatography media is at least a two-stage process. Application of pure protein pulses (bovine serum albumin and beta-lactoglobulin) to hydrophobic interaction chromatography media yielded two chromatographic peaks at low salt concentrations. At these salt concentrations, the adsorption process is affected by a second reaction, which can be interpreted as protein spreading or partial unfolding of the protein. The kinetic constants of the spreading reaction were derived from pulse response experiments at different residence times and varying concentrations by applying a modified adsorption model considering conformational changes. The obtained parameters were used to calculate uptake and breakthrough curves for spreading proteins. Although these parameters were determined at low saturation of the column, predictions of overloaded situations could match the experimental runs satisfactorily. Our findings suggest that proteins which are sensitive to conformational changes should be loaded at high salt concentrations in order to accelerate the adsorption reaction and to obtain steeper breakthrough curves.

Adsorption↗
PubMed2005

Epitope spreading within lupus-associated ribonucleoprotein antigens.

Autoantibodies reactive with several cellular antigens are present in the sera of patients with systemic lupus erythematosus. Polypeptides within the Ro-RNP complex and the snRNP complex are often targeted by these autoantibodies. One of the mechanisms responsible for their evolution is that of epitope spreading. Experimental animal model systems provide evidence for this. This review discusses the animal model systems of epitope spreading within these ribonucleoprotein antigens, the mechanisms of epitope spreading, and its relevance for disease pathogenesis.

Animals↗
PubMed2004

Endocytosis controls spreading and effective signaling range of Fgf8 protein.

Secreted signaling molecules released from a restricted source are of great importance during embryonic development because they elicit induction, proliferation, differentiation, and patterning events in target cells . Fgf8 is a member of the fibroblast growth factor family with key inductive functions during vertebrate development of, for example, the forebrain , midbrain , cerebellum , heart , inner ear , and mesoderm . However, the mechanism by which the signaling range of Fgf8 is controlled in a field of target cells is unknown. We studied Fgf8 as a potential morphogen in the nascent neuroectoderm of living zebrafish embryos. We find that spreading of epitope-tagged Fgf8 through target tissue is carefully controlled by endocytosis and subsequent degradation in lysosomes, or "restrictive clearance," from extracellular spaces. If internalization is inhibited, Fgf8 protein accumulates extracellularly, spreads further, and activates target gene expression over a greater distance. Conversely, enhanced internalization increases Fgf8 uptake and shortens its effective signaling range. Our results suggest that Fgf8 spreads extracellularly by a diffusion-based mechanism and demonstrate that target cells can actively influence, through endocytosis and subsequent degradation, the availability of Fgf8 ligand to other target cells.

Animals↗
PubMed2006

NR2B antagonists restrict spatiotemporal spread of activity in a rat model of cortical dysplasia.

Freeze-lesion-induced focal cortical dysplasia in rats closely resembles human microgyria, a neuronal migration disorder associated with drug-resistant epilepsy. Alterations in expression of N-methyl-D-aspartate receptors (NMDARs) containing NR2B subunits have been suggested to play a role in the hyperexcitability seen in this model. We examined the effect of NMDAR antagonists selective for NR2B subunits (Ro 25-6981 and ifenprodil) on activity evoked by intracortical stimulation in brain slices from freeze-lesioned rat neocortex. Whole-cell voltage-clamp recordings showed that Ro 25-6981 (1 microM) significantly reduced the response area of evoked postsynaptic currents in pyramidal cells from the paramicrogyral area whereas responses were unaffected in slices from control (sham operated) animals. Voltage-sensitive dye imaging was used to examine spatiotemporal spread of evoked activity in lesioned and control cortices. The imaging experiments revealed that peak amplitude, duration, and lateral spread of evoked activity in the paramicrogyral area was reduced by bath application of Ro 25-6981 (1 microM) and ifenprodil (10 microM). Ro 25-6981 had no effect on evoked activity in neocortical slices from control animals. The non-selective NMDAR antagonist d-2-amino-5-phosphonvaleric acid (APV, 20 microM) reduced activity evoked in presence of 50 microM 4-aminopyridine (known to increase excitability by enhancing neurotransmitter release) in neocortical slices from control animals whereas Ro 25-6981 (1 microM) did not. These results suggest that NR2B subunit-containing NMDARs contribute significantly to the enhanced spatiotemporal spread of paroxysmal activity observed in vitro in the rat freeze-lesion model of focal cortical dysplasia.

Adrenergic alpha-Antagonists↗
PubMed2005

Inhibition of cell spreading in CHO cells transfected with cDNA of a glycosylphosphatidyl inositol-anchored protein, GPI-80.

We have previously cloned a glycosylphosphatidyl inositol (GPI)-anchored protein, designated GPI-80 that associated with integrin and may modulate leukocyte adherence and migration. Recent studies have shown that GPI-80 belongs to a Vanin family that is related to pantetheinase, but the regulatory function of GPI-80 in cell adherence is still unclear. To clarify the possible functions of GPI-80, we transfected GPI-80 cDNA into Chinese hamster ovary (CHO) cells and observed adherence and morphological changes. Adherence of GPI-80 transfectants was significantly decreased when signal strength for the cell adhesion is weak, and the cell spreading of the transfectants was strongly inhibited. This inhibitory effect of GPI-80 expression was largely canceled by GPI-80 shedding with phosphatidy-linositol-specific phospholipase C. Interestingly, spreading of GPI-80 transfectants was temporarily recovered from the round shape but not maintained by stimulation with known activators of beta1 integrins, phorbol myristate acetate and manganese ions. Taken together, these results suggest that the expression of GPI-80 on CHO cells can influence cell spreading in weak adhesive signal conditions via extracellular matrix molecules.

Amidohydrolases↗
PubMed2004

Traction in smooth muscle cells varies with cell spreading.

Changes in cell shape regulate cell growth, differentiation, and apoptosis. It has been suggested that the regulation of cell function by the cell shape is a result of the tension in the cytoskeleton and the distortion of the cell. Here we explore the association between cell-generated mechanical forces and the cell morphology. We hypothesized that the cell contractile force is associated with the degree of cell spreading, in particular with the cell length. We measured traction fields of single human airway smooth muscle cells plated on a polyacrylamide gel, in which fluorescent microbeads were embedded to serve as markers of gel deformation. The traction exerted by the cells at the cell-substrate interface was determined from the measured deformation of the gel. The traction was measured before and after treatment with the contractile agonist histamine, or the relaxing agonist isoproterenol. The relative increase in traction induced by histamine was negatively correlated with the baseline traction. On the contrary, the relative decrease in traction due to isoproterenol was independent of the baseline traction, but it was associated with cell shape: traction decreased more in elongated than in round cells. Maximum cell width, mean cell width, and projected area of the cell were the parameters most tightly coupled to both baseline and histamine-induced traction in this study. Wide and well-spread cells exerted larger traction than slim cells. These results suggest that cell contractility is controlled by cell spreading.

Adhesiveness↗
PubMed2004

Spreading of nanofluids driven by the structural disjoining pressure gradient.

This paper discusses the role of the structural disjoining pressure exerted by nanoparticles on the spreading of a liquid film containing these particles. The origin of the structural disjoining pressure in a confined geometry is due to the layering of the particles normal to the confining plane and has already been traced to the net increase in the entropy of the system in previous studies. In a recent paper, Wasan and Nikolov (Nature, 423 (2003) 156) pointed out that the structural component of the disjoining pressure is strong enough to move a liquid wedge; this casts a new light on many applications-most notably, detergency. While the concept of spreading driven by the disjoining pressure is not new, the importance of the structural disjoining pressure arises from its long-range nature (as compared to the van der Waals' force), making it an important component of the overall force balance near the contact line. In this paper, we report on a parametric study of the spreading phenomena by examining the effects of nanoparticle size, concentration and polydispersity on the displacement of an oil-aqueous interface with the aqueous bulk containing nanoparticles. The solution of the extended Laplace-Young equations for the profile of the meniscus yields the position of the nominal contact line under the action of the structural disjoining pressure. Simulations show that the displacement of the contact line is greater with a high nanoparticle volume fraction, small particles for the same volume fraction, monodispersed (in size) particles rather than polydispersed particles and when the resisting capillary pressure is small, i.e., when the interfacial tension is low and/or the radius of the dispersed phase drop/bubble is large.

Journal Article↗
PubMed2006

Spread of large LNG pools on the sea.

A review of the standard model of LNG pool spreading on water, comparing it with the model and experiments on oil pool spread from which the LNG model is extrapolated, raises questions about the validity of the former as applied to spills from marine tankers. These questions arise from the difference in fluid density ratios, in the multi-dimensional flow at the pool edge, in the effects of LNG pool boiling at the LNG-water interface, and in the model and experimental initial conditions compared with the inflow conditions from a marine tanker spill. An alternate supercritical flow model is proposed that avoids these difficulties; it predicts significant increase in the maximum pool radius compared with the standard model and is partially corroborated by tests of LNG pool fires on water. Wind driven ocean wave interaction has little effect on either spread model.

Accidents↗
PubMed2005

Changing pattern of hepatitis C virus spread in rural areas of Egypt.

BACKGROUND/AIMS: To identify patterns of HCV spread in the Nile Delta of Egypt. METHODS: Residents in a Nile Delta village were invited to participate in a cohort study of HCV infection. Risk factors for past or current infection were identified at cohort intake using generalized estimated equations models. Attributable fractions were calculated for all independent risk factors. RESULTS: The prevalence of HCV antibodies increased from 2.7% in those <20 years of age to more than 40% in males aged 40-54 years. The peak in HCV prevalence in the 40-54 year age group corresponds to the aging of the cohort of children infected through schistosomiasis intravenous treatments in the 1960s-70s (accounting for 12.4% of all HCV infections observed today among adults). Following this initial founding event, the HCV epidemic has spread in the community through iatrogenic factors, and particularly injections (37.9% of the overall attributable fraction in adults). In children, however, no iatrogenic factors were associated with increased risk of infection, suggesting a change in the pattern of HCV spread. CONCLUSIONS: While HCV infections in adults could be attributed to iatrogenic factors, and particularly injections, infections in children could not be explained by similar routes of transmission.

Adolescent↗