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PubMed1983

Quantification of the degree of cell spreading of human fibroblasts by semi-automated analysis of the cell perimeter.

Cell flattening and spreading on a substratum is of major importance in cellular and developmental biology. To study the mechanisms of cell spreading, quantitative and reproducible measures of the degree of cell spreading must be available. Normal human fibroblasts, spreading on a substratum, were fixed with glutaraldehyde, stained with acridine orange and photographed (X 40) under a fluorescence microscope. The photonegatives (containing 10-30 cells) were scanned with a drum scanner and a complete picture containing 128 gray levels was constructed. Each cell contour was calculated with the use of a local threshold. The image and the superimposed cell contours were displayed on a television screen (16 gray levels) and errors were corrected interactively. With this system the spreading of normal human skin fibroblasts as a function of time could be quantified reproducibly. Compared to surface area or shape, the cell perimeter proved to be a very sensitive parameter of the degree of spreading. By using cell perimeter measurements, differences in the degree of spreading on various substrata could be quantified.

Acridine Orange↗

PubMedDate not supplied

Patterns of spread of squamous cell carcinoma within the mandible.

The patterns of spread of squamous cell carcinoma within the mandible were investigated in 43 nonirradiated (33 edentulous and 10 partially dentate) and 16 irradiated mandibles. Two modes of spread were identified: (1) spread in relation to the inferior alveolar nerve, and (2) spread in spaces between cancellous bony trabeculae. Although nerve-related spread was significantly more frequent in the edentulous than in the partially dentate nonirradiated mandible, the difference in incidence between all nonirradiated mandibles and irradiated mandibles was not significant. The patterns of spread in cancellous bone in irradiated and nonirradiated mandibles differed little. Spread of tumor within the medulla, deep to an intact cortex beyond the extent of extraosseous soft tissue tumor, was seen infrequently.

Carcinoma, Squamous Cell↗

PubMed1994

Phorbol ester induced rapid attachment and spreading of melanoma cells and the role of extracellular matrix proteins.

Phorbol 12-myristate 13-acetate (PMA) is a tumour promotor that acts as a potent protein kinase C (PKC) activator that has significant effects on tumour cell attachment and spreading. We tested whether these effects of PMA may be observed in human melanoma cells, and whether a specific response to extracellular matrix proteins may be mediated by shifts in the expression of beta 1 integrins. We used cell attachment assays, video time lapse cell spreading assays, flow cytometry, function blocking monoclonal antibodies (MAbs) and PKC inhibitor Calphostin C to address these questions. We established that PMA induces a rapid and temporary enhancement of cell attachment and spreading which was not accompanied by a significant change in the expression of beta 1 integrins. Spreading of melanoma cells that were not stimulated with PMA could be significantly blocked with a function blocking MAb (clone P4C10) against the common beta 1 integrin subunit. The spreading and attachment of the PMA treated cells was also significantly reduced, but less so, after MAb treatment. The PMA enhanced cell attachment and spreading could be effectively blocked by RGD sequences and PKC inhibitor. Taken together, our data indicate that PMA induces a rapid and temporary ECM-dependent enhancement of melanoma cell attachment and spreading, and that the response to ECM components appears not to be due to significant shifts in beta 1 integrin expression, but rather to activation of beta 1 integrins.

Amino Acid Sequence↗

PubMed1981

Trifluoperazine inhibits spreading and migration of cells in culture.

Trifluoperazine (TFP) blocks spreading and migration of cultured mammalian cells. These are calcium-dependent and microfilament-mediated processes. Calmodulin, a regulator of many calcium-dependent processes in cells, is selectively inhibited by TFP. Cell spreading on a plastic- or collagen-coated substratum was reversibly inhibited by 10 micro M TFP. The drug blocks cell spreading even in the presence of 1 mM cAMP. TFP is as effective as cytochalasin B (CB), in inhibitor of microfilament function, in blocking cell spreading. All cell lines tested, whether "normal" or virally transformed, failed to spread to TFP. The drug, at a concentration sufficient to inhibit spreading, does not interfere with the initial attachment of a cell to a plastic surface. Cells plated in the presence of 10 micro M TFP attach at a rate and to an extent equal to untreated controls. TFP added to already spread cells results in a reversible cell rounding. Detection of fibronectin by indirect immunofluorescence suggests TFP-induced cell rounding is not due to shedding of fibronectin from the cell surface. TFP reversibly blocks cell migration into a would edge almost as effectively as CB. We suggest that TFP interferes with these microfilament-mediated functions by direct action on the microfilaments or indirect action by inactivating calmodulin.

Animals↗

PubMed2003

Clinicopathological characteristics of superficial spreading type early gastric cancer.

BACKGROUND AND OBJECTIVES: Superficial spreading type early gastric cancer is characterized by its atypical growth pattern and occasionally indistinct tumor margin. Because it is a rare form of early gastric cancer, the clinicopathological details are not apparent. The aim of this study was to clarify the clinicopathological features of the superficial spreading type of early gastric cancer. METHODS: A retrospective study was conducted in 1,062 surgically resected patients with early gastric cancer. Hospital records were compared between patients with superficial spreading type early gastric cancer and those with more common types of early gastric cancer. RESULTS: Sixty-nine patients (6.9%) had superficial spreading lesions. The male to female ratio was 1.2:1. The most frequent histological type was signet-ring cell carcinoma (32%). The distinguishing histopathological features were submucosal invasion (67%), lymphatic invasion (32%), and lymph node metastasis (30%). There were discrepancies in tumor area between surgical findings and pathological diagnosis in 24 patients (35%) with superficial spreading type. More extensive lymph node dissection was performed and all patients survived in the group with superficial spreading lesions. CONCLUSIONS: The most appropriate treatment for the superficial spreading type of early gastric cancer is wide surgical resection with extensive lymph node dissection.

Female↗

PubMed1981

Interaction of serum and cell spreading affects the growth of neoplastic and non-neoplastic fibroblasts.

Both growth factor availability and cell-to-cell contact have been mechanisms used to explain cell growth regulation at high cell density. Recently Folkman and colleagues have shown that changes in cell shape, rather than cell-to-cell contact, can regulate the growth of fibroblasts. However, in those studies the relation between serum and shape regulation of growth was not studied, nor were neoplastic and non-neoplastic cells compared. In this report we have studied these aspects by varying cell spreading and serum concentration independently for 2 non-neoplastic and 3 neoplastic cell lines. Cell spreading (projected cell area) was controlled by decreasing the adhesiveness of tissue culture growth was measured as the increase in cell number/day. We have found that more spreading increased net growth of both neoplastic and non-neoplastic cells, while less spreading (toward rounded configuration) depressed growth. There were also quantitative differences between neoplastic and non-neoplastic cells. Neoplastic cells continued to grow under conditions of cell rounding, which completely prevented the growth of their non-neoplastic counterparts. Some neoplastic cells also tended to show little or no increase in net cell number for serum concentrations above 10% as cells became more spread; in contrast, all non-neoplastic cells grew more with increasing concentrations of serum as they became well spread. Thus, in normal cells, it appears that the sensitivity of cells to humoral factors is governed by cell spreading. This interaction between serum and cell shape is less prominent in some neoplastic cells.

Animals↗

PubMed1997

Laminin reduces HSV-1 spread from cell to cell in human keratinocyte cultures.

Herpes simplex virus-1 (HSV-1) infects epidermal cells where it replicates and spreads from cell to cell. While some of the viral factors responsible for cell-to-cell spread are known, the host cell molecules and structures which are utilized by HSV-1 during spread are not well studied. Here we report that a laminin substrate reduced the ability of HSV-1 to spread from cell to cell in cultures of a human keratinocyte cell line (HaCaT). Laminin did not reduce spread of the virus by decreasing the viral replication rate. However, laminin did stimulate the formation of tight junctions between HaCaT cells, suggesting that tight junctions can affect cell-to-cell spread of HSV-1. Since laminin is an abundant component of the basement membrane in vivo, culturing cells on laminin may provide an assay which more accurately reflects the rate and mechanism of HSV-1 cell-to-cell spread in vivo.

Animals↗

PubMed2000

Colon cancer cells adhesion and spreading on autocrine laminin-10 is mediated by multiple integrin receptors and modulated by EGF receptor stimulation.

Epidermal growth factor (EGF) receptor ligands such as EGF and transforming growth factor-alpha (TGF-alpha) play an important role in controlling the proliferation, survival, morphology, and motility of colonic epithelial cells. There is also increasing evidence that growth factors and extracellular matrix (ECM) proteins cooperate to regulate these cellular processes. We have reported previously that autocrine TGF-alpha and an unidentified ECM protein in the serum-free conditioned medium of the human colon carcinoma cell line LIM1215 synergize to induce spreading of these cells in low-density cultures. We have now purified the ECM protein secreted by LIM1215 cells and show that it synergizes with EGF to induce spreading of LIM1215 cells and other human cell lines from the colon and other tissues. The purified ECM migrated as a single protein band with an apparent molecular mass of approximately 800 kDa on SDS-PAGE under nonreducing conditions and, under reducing conditions, as three protein bands of approximately 360, 210, and 200 kDa. Immunoblotting experiments and mass spectrometry analysis of tryptic digests on the purified protein identified the 360-, 210-, and 200-kDa protein bands as laminin alpha5, beta1, and gamma1 chains, respectively, indicating that LIM1215 cells secrete laminin-10 (alpha5 beta1 gamma1). In serum-free medium, LIM1215 cells adhere to laminin-10 primarily via alpha2 beta1 and alpha3 beta1 integrin receptors. EGF-induced spreading of LIM1215 cells on laminin-10 is partially inhibited by pretreatment of the cells with blocking antibodies directed against integrin alpha3 or beta1 but not alpha2, alpha6, or beta4 subunits. Spreading is almost completely inhibited by blocking alpha3 + alpha2, alpha3 + alpha6, or beta1 + beta4 integrin chains and results in cell death. Increased spreading in the presence of EGF correlates with up-regulation of alpha6 beta4 integrins in these cells after exposure to EGF. These results indicate that colon cancer cells attach and spread on laminin-10 via multiple integrin receptors and suggest a critical role for alpha3 beta1 integrins in the spreading response. Together, our results support the concept that the adhesive properties of colon cancer cells are modulated by autocrine production of TGF-alpha and laminin-10 and autocrine induction of appropriate integrins.

Amino Acid Sequence↗

PubMed1996

Capillarity Effects on Viscous Gravity Spreadings of Wetting Liquids.

Highly viscous silicone oils within a wide range of volumes were left to spread on smooth horizontal substrates to investigate the effects of capillarity on viscous gravity spreadings under the condition of complete wetting. The study was centered on the intermediate asymptotic behavior, where the details of the initial liquid distribution are irrelevant. We detected small but appreciable departures from the well-known solution without surface tension forces (viscous gravity self similar solution, or base solution). Two stages are clearly identified in the spreadings. During the first, which is usually rather brief, capillarity does not play an appreciable role on the dynamics of the spreading, i.e., the base solution is a very good approximation. The head of the current displays a wheel-like profile progressively decreasing in size; when the size becomes on the order of the capillary length, this stage ends. The wheel-like configuration cannot be associated either with the rheological behavior of the fluid used or with the initial conditions. To observe this first stage without the influences due to peculiarities of the initial conditions, a proper release of the spreading is needed. The second stage is characterized by a spreading rate below the base solution; the slowing is associated with a change of the current head shape, which takes the form of a wedge as a consequence of capillarity. The rate of advance of the front may still be well approximated by the same power law as given by the base solution, but with a smaller prefactor. In this work we measure the parameters that characterize the flow during both stages; besides, for the second stage, we develop a heuristic calculation which shows that the wedge-like shape of the current head gives place to a higher viscous dissipation rate, thus explaining the observed slowing of the spreading.

Journal Article↗

PubMed1997

Effect of the Spreading Coefficient on Three-Phase Flow in Porous Media

A pore-level network model has been developed to study the effect of spreading coefficients on three-phase flow through porous media. This model combines the morphological description of the pore space with pore-level displacement physics to model capillarity-controlled, immiscible gas invasion of a porous medium initially saturated with water and oil. Three displacement events are involved during gas invasion, namely, direct water drainage, direct oil drainage, and double drainage. Direct oil drainage and double drainage involve oil mobilization and consequently lead to oil recovery. Direct water drainage event is preferred over double drainage if the spreading coefficient is highly negative. The residual oil saturation to gasflood starting after a waterflood is higher for nonspreading oils than for spreading oils. In spreading oils, it is not a function of the spreading coefficient. In nonspreading oils, the residual oil saturation increases with the magnitude of the spreading coefficient. The residual oil saturation to gasflood is also a function of the initial oil saturation; it increases as the initial oil saturation increases. The increase is higher for nonspreading oils. The gas-oil capillary pressure is not a function of the liquid saturation alone, as is commonly presumed. It is a function of the spreading coefficient and the initial oil saturation, as well.

Journal Article↗

PubMed2002

Spreading of liquid drops over saturated porous layers.

Spreading of small liquid drops over thin porous layers saturated with the same liquid is investigated from both theoretical and experimental points of view. A theory is presented that shows that spreading is governed by the same power law as in the case of spreading over a dry solid substrate. The Brinkman's equations are used to model the liquid flow inside the porous substrate. An equation of the drop spreading is deduced, which shows that both an effective lubrication and the liquid exchange between the drop and the porous substrates are equally important. The presence of these two phenomena removes the well-known singularity at the moving three-phase contact line. Matching of the drop profile in the vicinity of the three-phase contact line with the main spherical part of the drop gives the possibility to calculate the pre-exponential factor in the spreading law via permeability and effective viscosity of the liquid in the porous layer. Unfortunately, the latter dependency turns out to be very weak. Spreading of silicone oils over different microfiltration membranes is carried out. Radii of spreading on time experimental dependencies confirm the theory predictions. Experimentally found coefficients agree with theoretical estimations.

Journal Article↗

PubMed1997

Control of methylation spreading in synthetic DNA sequences by the murine DNA methyltransferase.

Methylation spreading, which involves a propensity for the mammalian DNA-(cytosine-5)-methyltransferase to de novo methylate cytosine-guanine dinucleotides (CpGs) near pre-existing 5-methylcytosine bases, has been implicated in the control of numerous biological processes. We have assessed methylation spreading by the murine DNA methyltransferase in vitro using synthetic copolymers and oligonucleotides which differ only in their methylation state. Double-stranded oligonucleotides were found to undergo higher levels of de novo methylation overall than otherwise identical single-stranded oligonucleotides. This difference reflects the greater number of de novo methylatable cytosine bases in double-stranded than single-stranded sequences. All tested oligonucleotides containing pre-existing 5-methyl-cytosine(s) were de novo methylated at several fold the rates of non-methylated controls. No mammalian proteins besides the DNA methyltransferase were required for this observed enhancement of de novo methylation. Studies using oligonucleotides differing in patterns of pre-methylation showed that methylation spreading can be initiated by hemimethylated or duplex methylated CpGs indicating that recognition of 5-methylcytosine by the enzyme is sufficient to stimulate methylation spreading. Double and single-stranded oligonucleotides with several bases between CpGs underwent considerably more de novo methylation per CpG than sequences containing sequential uninterrupted methylatable sites. Spacing preferences by the DNA methyltransferase were also observed in hemimethylated oligonucleotides, suggesting that this is a general property of the enzyme. Although methylation spreading outside of CpG dinucleotides was relatively rare, single-stranded DNA incurred higher levels of de novo methylation at sites other than CpG as compared to double-stranded DNA. This indicates less specificity of methylation spreading in single-stranded sequences. Finally, enhanced de novo methylation in the presence of fully methylated CpG sites in double-stranded oligonucleotides was not as high as the rates of methylation of hemimethylated CpGs in otherwise identical oligonucleotides. These studies provide further elucidation of the mechanisms and regulation of the methylation spreading process and its potential role in the biological processes it influences.

5-Methylcytosine↗

PubMed1995

MHVR-independent cell-cell spread of mouse hepatitis virus infection requires neutral pH fusion.

Receptor-specificity is a key determinant of viral tropism. In this report, however, we have demonstrated that cell-associated spread of MHV can bypass the requirement for binding to primary receptors and thereby spread to cells that are resistant to MHV infection. Anti-receptor antibody CC1, which blocks infection by MHV virions, failed to prevent cell-associated spread of MHV to receptor-negative BHK cells or receptor-positive DBT cells. Cell-associated MHV may be utilizing an alternative, low-affinity receptor that is inadequate for functional interaction with MHV virions. Theoretically, dissemination of MHV infection through a receptor-independent, cell-associated mechanism in vivo provides the potential for broader host and tissue range, and for spread of infection despite the presence neutralizing antibodies. Receptor-independent, cell-associated spread of MHV requires neutral pH fusion capability. The low pH-dependent MHV variant OBLV60, which utilizes an endocytic route of entry, does not spread through a receptor-independent mechanism. Additionally, antiviral antibodies that block MHV spike-mediated fusion inhibited cell-associated spread of infection.

Animals↗

PubMed1994

Prolyl hydroxylase inhibitor and lysyl hydroxylase inhibitor inhibit spreading of corneal epithelium.

BACKGROUND: The spreading of epithelium is critical in the healing of corneal wounds. Such epithelial spreading requires the continuous production of protein and glycoprotein. To determine whether collagen production is required for the spreading of corneal epithelium, we studied the effects of inhibitors for collagen production on spreading of corneal epithelium in vitro. METHODS: We examined the effect of two proline analogs, L-azetidine 2-carboxylic acid and cis-hydroxyproline, a prolyl hydroxylase inhibitor, ethyl-3,4-dihydroxybenzoate, and a lysyl hydroxylase inhibitor, minoxidil, on the spreading of epithelium of organ-cultured rabbit cornea. RESULTS: Both analogs and inhibitors inhibited epithelial spreading in a dose-dependent manner. CONCLUSION: These observations indicate that collagen production may be involved in the spreading of corneal epithelium.

Animals↗

PubMed1986

Analysis of spreading of inactivation in eight X autosome translocations utilizing the high resolution RBG technique.

Eight X autosome translocations were studied with replication banding to localize spreading of late replication into the autosomal segments. Partial spreading into the autosomal segment was seen in four translocations and no spreading of late replication was seen in four translocations. In those translocations with partial spreading of late replication into the autosomal segment, late replication did not always spread continuously from the X chromosome breakpoint throughout the autosome. Instead, it appeared to skip some bands and affect others. The data on the pattern of replication, taken to indicate also a spread of inactivation into these autosomal segments, correlated well with the clinical data in most cases and suggest that spreading of late replication is often incomplete and may be discontinuous.

Chromosome Banding↗

PubMedDate not supplied

The spread of human lung cancer cells on collagens and its inhibition by type III collagen.

The cell spreading ability of human lung cancer cells on collagen substrata was examined in comparison with normal human tracheal epithelial cells. Plastic dishes or multiwells were coated with type I, III or IV collagen gel at a concentrate of 200 micrograms/cm2. Ninety per cent of the normal cells were round on all collagens. Adenocarcinoma RERF-LC-MS and VMRC-LCD cell lines and squamous cell carcinoma VMRC-LCP cell line, which metastasize weakly after intrasplenic transplantation in nude mice, spread relatively poorly. Adenocarcinoma, A549 and SK-LU-1 and squamous cell carcinoma Calu-1 cell lines, which were highly metastatic to liver, spread well. Adenocarcinoma ABC-1 cell line, which is moderately metastatic to liver in nude mice, spread moderately. On type III collagen, three adenocarcinoma cell lines (A549, ABC-1 and VMRC-LCD) gradually started to contract after initial spreading and became round at 24 h. These results suggest that there may be a correlation between the degree of malignancy of human lung cancer cells and their spreading ability on collagen substrata, and that the cell spreading ability may be regulated by type III collagen in some lung cancer cells.

Adenocarcinoma↗

PubMed1996

Preoperative detection of distal intramural spread of lower rectal carcinoma using transrectal ultrasonography.

PURPOSE: Usefulness of transrectal ultrasonography (TRUS) for detecting distal intramural spread of rectal carcinoma was investigated. METHODS: Thirty-seven patients with advanced rectal carcinoma, who had not received preoperative adjuvant therapy, underwent TRUS before surgery. Distal intramural spread was evaluated by TRUS and by pathologic examination of resected specimens. RESULTS: Distal intramural spread was found in 7 of 37 patients (19 percent) by pathologic examination. Presence or absence of distal intramural spread was correctly diagnosed by TRUS in 86 percent of the 37 patients. Misdiagnosis by TRUS mainly occurred when distal intramural spread was 5 mm. Tumor penetration of muscularis propria, lymph node involvement, and a higher histologic grade of malignancy showed a significant relationship with the presence of distal intramural spread. CONCLUSION: TRUS was useful for detecting distal intramural spread > 5 mm in patients with lower rectal carcinoma and may be helpful for selecting appropriate surgery.

Adenocarcinoma↗

PubMed1999

Changes in the mechanical properties of fibroblasts during spreading: a micromanipulation study.

Cell morphology is controlled in part by physical forces. If the main mechanical properties of cells have been identified and quantitated, the question remains of how the cell structure specifically contributes to these properties. In this context, we addressed the issue of whether cell rheology was altered during cell spreading, taken as a fundamental morphological change. On the experimental side, we used a novel dual micromanipulation system. Individual chick fibroblasts were allowed to spread for varying amounts of time on glass microplates, then their free extremity was aspirated into a micropipet at given pressure levels. Control experiments were also done on suspended cells. On the theoretical side, the cell was modeled as a fluid drop of viscosity mu, bounded by a contractile cortex whose tension above a resting value was taken to be linearly dependent on surface area expansion. The pipet negative pressure was first adjusted to an equilibrium value, corresponding to formation of a static hemispherical cap into the pipet. This allowed computation, through Laplace's law, of the resting tension (tau 0), on the order of 3 x 10(-4) N/m. No difference in tau 0 was found between the different groups of cells studied (suspended, adherent for 5 min, spread for 0.5 h, and spread for 3 h). However, tau 0 was significantly decreased upon treatment of fibroblasts with inhibitors of actin polymerization or myosin function. Then, the pressure was set at 30 mmH2O above the equilibrium pressure. All cells showed a biphasic behavior: (1) a rapid initial entrance corresponding to an increase in surface area, which was used to extract an area expansion elastic modulus (K), in the range of 10(-2) N/m; this coefficient was found to increase up to 40% with cell spreading; (2) a more progressive penetration into the pipet, linear with time; this phase, attributed to viscous behavior of the cytoplasm, was used to compute the apparent viscosity (mu, in the range of 2-5 x 10(4) Pa s) which was found to increase by as much as twofold with cell spreading. In some experiments the basal force at the cell-microplate interface was quantitated with flexible microplates and found to be around 1 nN, in agreement with values calculated from the model. Taken together, our results indicate a stiffening of fibroblasts upon spreading, possibly correlated with structural organization of the cytoskeleton during this process. This study may help understand better the morphology of fibroblasts and their mechanical role in connective tissue integrity.

Actins↗