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PubMed2004

Spreading dilatation in rat mesenteric arteries associated with calcium-independent endothelial cell hyperpolarization.

Both ACh and levcromakalim evoke smooth muscle cell hyperpolarization and associated relaxation in rat mesenteric resistance arteries. We investigated if they could evoke conducted vasodilatation along isolated arteries, whether this reflected spreading hyperpolarization and the possible mechanism involved. Focal micropipette application of either ACh, to stimulate endothelial cell muscarinic receptors, or levcromakalim, to activate smooth muscle K(ATP) channels, each evoked a local dilatation (88 +/- 14%, n= 6 and 92 +/- 6% reversal of phenylephrine-induced tone, n= 11, respectively) that rapidly spread upstream (at 1.5 mm 46 +/- 19%, n= 6 and 57 +/- 13%, n= 9) to dilate the entire isolated artery. The local dilatation to ACh was associated with a rise in endothelial cell [Ca(2+)](i) (F/F(t = 0)= 1.22 +/- 0.33, n= 14) which did not spread beyond 0.5 mm (F/F(t = 0)= 1.01 +/- 0.01, n= 14), while the local dilatation to levcromakalim was not associated with any change in endothelial cell [Ca(2+)](i). In contrast, ACh and levcromakalim both stimulated local (12.7 +/- 1.2 mV, n= 10 and 13.5 +/- 4.7 mV, n= 10) and spreading (at 2 mm: 3.0 +/- 1.1 mV, n= 5 and 4.1 +/- 0.7 mV, n= 5) smooth muscle hyperpolarization. The spread of hyperpolarization could be prevented by cutting the artery, so was not due to a diffusible agent. Both the spreading dilatation and hyperpolarization were endothelium dependent. The injection of propidium iodide into either endothelial or smooth muscle cells revealed extensive dye coupling between the endothelial cells, but limited coupling between the smooth muscle cells. Some evidence for heterocellular spread of dye was also evident. Together, these data show that vasodilatation can spread over significant distances in mesenteric resistance arteries, and suggest this reflects an effective coupling between the endothelial cells to facilitate [Ca(2+)](i)-independent spread of hyperpolarization.

Acetylcholine↗
PubMed1998

A tensegrity model of the cytoskeleton in spread and round cells.

Measurements on adherent cells have shown that spreading affects their mechanics. Highly spread cells are stiffer than less spread cells. The stiffness increases approximately linearly with increasing applied stress and more so in highly spread cells than in less spread cells. In this study, a six-strut tensegrity model of the cytoskeleton is used to analyze the effect of spreading on cellular mechanics. Two configurations are considered: a "round" configuration where a spherically shaped model is anchored to a flat rigid surface at three joints, and a "spread" configuration, where three additional joints of the model are attached to the surface. In both configurations a pulling force is applied at a free joint, distal from the anchoring surface, and the corresponding deformation is determined from equations of equilibrium. The model stiffness is obtained as the ratio of applied force to deformation. It is found that the stiffness changes with spreading consistently with the observations in cells. These findings suggest the possibility that the spreading-induced changes of the mechanical properties of the cell are the result of the concomitant changes in force distribution and microstructural geometry of the cytoskeleton.

Cell Adhesion↗
PubMed1995

Glycoproteins E and I facilitate neuron-to-neuron spread of herpes simplex virus.

Two herpes simplex virus (HSV) glycoproteins E and I (gE and gI) form a heterooligomer which acts as an Fc receptor and also facilitates cell-to-cell spread of virus in epithelial tissues and between certain cultured cells. By contrast, gE-gI is not required for infection of cells by extracellular virus. HSV glycoproteins gD and gJ are encoded by neighboring genes, and gD is required for both virus entry into cells and cell-to-cell spread, whereas gJ has not been shown to influence these processes. Since HSV infects neurons and apparently spreads across synaptic junctions, it was of interest to determine whether gD, gE, gI and gJ are also important for interneuronal transfer of virus. We tested the roles of these glycoproteins in neuron-to-neuron transmission of HSV type 1 (HSV-1) by injecting mutant viruses unable to express these glycoproteins into the vitreous body of the rat eye. The spread of virus infection was measured in neuron-rich layers of the retina and in the major retinorecipient areas of the brain. Wild-type HSV-1 and a gJ- mutant spread rapidly between synaptically linked retinal neurons and efficiently infected major retinorecipient areas of the brain. gD mutants, derived from complementing cells, infected only a few neurons and did not spread in the retina or brain. Mutants unable to express gE or gI were markedly restricted in their ability to spread within the retina, produced 10-fold-less virus in the retina, and spread inefficiently to the brain. Furthermore, when compared with wild-type HSV-1, gE- and gI- mutants spread inefficiently from cell to cell in cultures of neurons derived from rat trigeminal ganglia. Together, our results suggest that the gE-gI heterooligomer is required for efficient neuron-to-neuron transmission through synaptically linked neuronal pathways.

Animals↗
PubMed1995

Cell spreading and the regulation of ornithine decarboxylase.

The aim of this study was to investigate the effect of cell spreading on the induction of ornithine decarboxylase and the rate of putrescine uptake in anchorage-dependent and anchorage-independent cells. Plating non-transformed IEC-6 epithelial cells at high versus low cell density restricted cell spreading from 900 microns 2 to approximately 140 microns 2, blunted the transient induction of ornithine decarboxylase activity from 202 to 32 pmol 14CO2/mg protein per hour and reduced the rate of [14C] putrescine uptake from 46 to 23 pmol/10(5) cells per hour. The mean spreading area of the cell population was controlled by coating tissue culture dishes with the nonadhesive polymer, polyHEMA. Ornithine decarboxylase activity and putrescine uptake correlated with cell spreading with minimal spreading (263 microns 2) corresponding to an 83% decrease in ornithine decarboxylase activity and 51% decrease in the rate of putrescine uptake. Adding the RGD peptide, Gly-Arg-Gly-Glu-Ser-Pro to the medium of sparsely plated cells resulted in rapid reductions in cell spreading concomitant with dose-dependent decreases in ornithine decarboxylase activity and putrescine uptake. Finally, minimizing cell spreading by depriving cells of substratum contact completely abolished serum-induced increases in ornithine decarboxylase and reduced the rate of putrescine uptake by 47%. In contrast to IEC-6 cells, ornithine decarboxylase of neoplastic HTC-116 cells was constitutively expressed with basal and stimulated activity (193 and 982 pmol 14CO2/mg protein per hour, respectively) completely independent of cell adhesion. Putrescine uptake, however, was abolished in the absence of cell adhesion. These data suggest that the induction of ornithine decarboxylase activity and the rate of putrescine uptake correlate with spreading of anchorage-dependent IEC-6 cells and that ornithine decarboxylase activity but not putrescine uptake, appears to be independent of spreading of neoplastic HTC-116 cells.

Cell Adhesion↗
PubMed1995

Dynamics of fibroblast spreading.

A new technique of microinterferometry permits cellular growth and motile dynamics to be studied simultaneously in living cells. In isolated chick heart fibroblasts, we have found that the non-aqueous mass of each cell tends to increase steadily, with minor fluctuations, throughout the cell cycle. The spread area of each cell also tends to increase during interphase but fluctuates between wide limits. These limits are dependent on the cell's mass and the upper limit is particularly sharp and directly proportional to mass. From a dynamical point of view, the spread area of a cell is determined by the balance between the rates of two antagonistic processes: protrusion of cellular material into new territory and retraction of material from previously occupied territory. The spatial asymmetry of these processes determines the translocation of the cell. We have found with the chick fibroblasts that the rates of the two processes are generally closely matched to each other and appear to be dependent on the cell's area of spreading. Both continue incessantly in well spread cells, even when there is no net translocation of the cell, and the lower limit of each activity is directly proportional to spread area. The two processes show different behaviour, however, during changes in the spread area of the cell. Both increases and decreases in area appear to be brought about by changes in the rate of retraction, the rate of protrusion remaining relatively constant. A simple stochastic model based on a limited supply of adhesion molecules can simulate all our observations including the mass-limited spreading, the strong correlation between protrusion and retraction and the retraction-dominated changes in area. We conclude that the spread area of the cell is actively regulated, possibly by a simple automatic mechanism that adjusts the area of spreading in relation to the mass of the cell and controls the rate of protrusion to compensate rapidly for spontaneous fluctuations in retraction.

Animals↗
PubMed2002

Sequential activation of individual PKC isozymes in integrin-mediated muscle cell spreading: a role for MARCKS in an integrin signaling pathway.

To understand how muscle cell spreading and survival are mediated by integrins, we studied the signaling events initiated by the attachment of muscle cells to fibronectin (FN). We have previously demonstrated that muscle cell spreading on FN is mediated by alpha5beta1 integrin, is associated with rapid phosphorylation of focal adhesion kinase and is dependent on activation of protein kinase C (PKC). Here we investigated the role of individual PKC isozymes in these cellular processes. We show that alpha, delta and epsilonPKC are expressed in muscle cells and are activated upon integrin engagement with different kinetics - epsilonPKC was activated early, whereas alpha and deltaPKC were activated later. Using isozyme-specific inhibitors, we found that the activation of epsilonPKC was necessary for cell attachment to FN. However, using isozyme-specific activators, we found that activation of each of three isozymes was sufficient to promote the spreading of alpha5-integrin-deficient cells on FN. To investigate further the mechanism by which integrin signaling and PKC activation mediate cell spreading, we studied the effects of these processes on MARCKS, a substrate of PKC and a protein known to regulate actin dynamics. We found that MARCKS was localized to focal adhesion sites soon after cell adhesion and that MARCKS translocated from the membrane to the cytosol during the process of cell spreading. This translocation correlated with different phases of PKC activation and with reorganization of the actin cytoskeleton. Using MARCKS-antisense cDNA, we show that alpha5-expressing cells in which MARCKS expression is inhibited fail to spread on FN, providing evidence for the crucial role of MARCKS in muscle cell spreading. Together, the data suggest a model in which early activation of epsilonPKC is necessary for cell attachment; the later activation of alpha or deltaPKC may be necessary for the progression from attachment to spreading. The mechanism of PKC-mediated cell spreading may be via the phosphorylation of signaling proteins, such as MARCKS, that are involved in the reorganization of the actin cytoskeleton.

Animals↗
PubMed1980

The distribution of cell-spreading activities in sera: a quantitative approach.

Sephacryl S-300 gel filtration of animal sera is used to demonstrate that there are at least 2 components that promote the 'spreading' of cells in culture. A morphometric technique is described to quantitate the spreading process. For a number of cell strains and established cell lines the more quantitatively significant spreading factor is not fibronectin. Rather it is a component with fibronectin and seems to cause spreading via a different mechanism from that stimulated by fibronectin. Thus fibronectin will cause spreading in the absence of protein synthesis, whereas the smaller component requires protein synthesis. The kinetics of spreading are also different at all concentrations of the factors that are effective. By comparing the spreading promoted by whole sera with that promoted by separate serum fractions following chromatography we conclude that under normal conditions plasma fibronectin plays little part in initial cell spreading. This view is supported by the fact that fibronectin-depleted serum will stimulate cell spreading.

Animals↗
PubMed1982

Qualitative and quantitative differences in spreading of human fibroblasts on various protein coats. Modulation by treatment of the cells with amines.

In contrast to established cell lines, normal human skin fibroblasts spread on their own fibronectin. The present investigation has examined whether human fibroblasts, like established cell lines, would be capable of spreading on substrata coated with proteins with different reactivity towards the cell surface. Coverslips were coated with human serum, fibronectin, alpha 2 macroglobulin-trypsin, a polyspecific anti-fibroblast antibody and a polyspecific anti-calf-serum antibody. The attachment of the cells to these substrate was of the same extent. Spreading was examined qualitatively using phase, interference contrast and reflection contrast optics on live cells, as well as scanning electron microscopy on fixed cells. To quantitate the maximum degree of cell spreading a semi-automated system was used, which measured the cell perimeter on a large number of cells. The distributions of the degree of cell spreading on the five substrata were compared statistically. The qualitative and quantitative differences observed on the various substrata could be further differentiated by adding various amines to the cells during 60 min spreading or during a 30 min preincubation before spreading. No strict correlation could be found between the effect of the amines on attachment or on spreading and their presumed effects on cellular transglutaminases. The results clearly indicate that the spreading of human fibroblasts can be modulated by the nature of the substratum and that, by using quantitative methods, these differences in behaviour can be measured accurately.

Cell Adhesion↗
PubMed1982

The abnormal morphology of polyoma-transformed baby hamster kidney cells is due to a failure to respond to 70K spreading factor.

The typical elongated bipolar morphology of baby hamster kidney (BHK) cells is not shown by polyoma-transformed BHK (Py-BHK) cells. Instead, the transformed line adheres poorly to tissue-culture plastic and cells have a more rounded morphology than the parent line. Plasma fibronectin is known to mediate the spreading of BHK cells, but when human serum is subjected to Sephacryl S-300 chromatography two peaks of spreading activity are eluted; the first is fibronectin and the second, which is quantitatively more significant, is a 70 K protein that is not related to fibronectin and stimulates spreading by a different mechanism. Py-BHK cells spread well in low concentrations of purified fibronectin but will not spread well in levels of serum that contain similar or greater concentrations of fibronectin. This is because fibronectin-mediated spreading of both BHK and Py-BHK cells occurs only in the presence of low concentrations of other proteins; albumin and other serum proteins inhibit fibronectin-mediated spreading. BHK cells spread under routine culture conditions in response to the 70 K factor rather than fibronectin. The altered morphology that results from viral transformation is due to a failure of the cells to respond to the 70 K spreading factor.

Animals↗
PubMed1982

Spreading of blastomeres from eight-cell mouse embryos on lectin-coated beads.

Single blastomeres from 8-cell embryos adhere to lectin-coated agarose beads. The cells spread over the surface of peanut lectin (PNA), wheat germ lectin (WGA) and concanavalin A (Con A)-coated agarose beads, and this was prevented by sugars with high affinity for the appropriate lectin. Spreading was also prevented by cytochalasin D at a concentration (0.5-1.0 microgram/ml) known to inhibit compaction of whole 8-cell embryos. Colcemid (1-2 micrograms/ml) only depressed spreading, as measured by linear contact distance, to 70-80% of that for the controls, while removal of calcium from the medium with EDTA had little effect on spreading. Fucose promoted spreading on WGA beads. Cells from 8-cell embryos will not adhere to negatively charged G-Sephadex and CM-Sephadex beads. They do adhere to positively charged DEAE-Sephadex beads but do not spread on them. In an attempt to inhibit cell spreading at compaction in intact 8-cell embryos, these were disaggregated in the presence of various (34) saccharide-containing molecules. Neither any sugar-containing molecules alone, nor combinations of N-acetyl-glucosamine, galactose and mannose, fucose and galactose, and fucose and lactose were able to inhibit compaction at physiological concentrations. However, blastocyst formation was inhibited to various extents by high nonphysiological concentrations (50 mM) of D-glucose, D-mannose, L-fucose, D-arabinose, N-acetyl-D-glucosamine, N-acetyl-D-galactosamine, alpha-lactose, 25 mM-alpha-melibionic acid and by 2 mg/ml fucoidin, ovine mucin and desialylated ovine mucin. Our results indicate that interaction of PNA, WGA and Con A with molecules on the cell surface that bind these lectins can trigger the cells to spread. However, a simple lectin-sugar interaction alone may not account for the spreading of cells on one another at compaction in whole 8-cell embryos.

Animals↗
PubMed2006

Potential impact of intermittent preventive treatment (IPT) on spread of drug-resistant malaria.

BACKGROUND: Treatment of asymptomatic individuals, regardless of their malaria infection status, with regularly spaced therapeutic doses of antimalarial drugs has been proposed as a method for reducing malaria morbidity and mortality. This strategy, called intermittent preventive treatment (IPT), is currently employed for pregnant women and is being studied for infants (IPTi) as well. As with any drug-based intervention strategy, it is important to understand how implementation may affect the spread of drug-resistant parasites. This is a difficult issue to address experimentally because of the limited size and duration of IPTi trials as well as the intractability of distinguishing the spread of resistance due to conventional treatment of malaria episodes versus that due to IPTi when the same drug is used in both contexts. METHODS AND FINDINGS: Using a mathematical model, we evaluated the possible impact of treating individuals with antimalarial drugs at regular intervals regardless of their infection status. We translated individual treatment strategies and drug pharmacokinetics into parasite population dynamic effects and show that immunity, treatment rate, drug decay kinetics, and presumptive treatment rate are important factors in the spread of drug-resistant parasites. Our model predicts that partially resistant parasites are more likely to spread in low-transmission areas, but fully resistant parasites are more likely to spread under conditions of high transmission, which is consistent with some epidemiological observations. We were also able to distinguish between spread of resistance due to treatment of symptomatic infections and that due to IPTi. We showed that IPTi could accelerate the spread of resistant parasites, but this effect was only likely to be significant in areas of low or unstable transmission. CONCLUSIONS: The results presented here demonstrate the importance of considering both the half-life of a drug and the existing level of resistance when choosing a drug for IPTi. Drugs to which little or no resistance exists are not advisable for IPT in high-transmission areas, but IPTi is not likely to significantly impact the spread of highly resistant parasites in areas where partial resistance is already established. IPTi is more likely to accelerate the spread of resistance in high-transmission areas than is IPT in adults (i.e., pregnant women).

Adult↗
PubMed2002

Effects of a plant sterol-enriched spread on serum lipids and lipoproteins in mildly hypercholesterolaemic subjects.

OBJECTIVE: In this randomized double-blind placebo-controlled cross-over study the effects of spreads enriched with plant sterols were determined on serum lipids, lipoprotein and apolipoprotein concentrations in a Belgian population. METHODS: Fourty-two healthy adult volunteers (22 men and 20 women) with an average age of 55 (SD 9) years and with serum total cholesterol concentrations below 300 mg/dl, consumed during two consecutive periods of 4 weeks two different low-fat spreads. Both the plant sterol rich and control spreads contained 35% of fat and had an almost equal fat composition. The sterol content of the enriched spread was 8.3%. Intake of the spreads was 25 g/day. RESULTS: Serum total and LDL-cholesterol concentrations lowered by 7% (18 mg/dl) and 10% (16 mg/dl), respectively, with the plant sterol-enriched compared to the control spread. Serum HDL-cholesterol concentration did not significantly differ between the two spreads. Apolipoprotein B concentrations lowered by 8% (0.08 g/l) with the plant sterol-enriched spread, while concentrations of apolipoprotein A-I did not change. CONCLUSION: These findings indicate that a daily intake of 25 gram low-fat spread containing 2 gram plant sterol per day is effective in lowering blood total and LDL cholesterol, and apolipoprotein B concentrations. This lowering may help to reduce the risk of heart disease in the population.

Adult↗
PubMed2001

Increased intracellular calcium is required for spreading of rat islet beta-cells on extracellular matrix.

Rat islet beta-cells spread in response to glucose when attached on the matrix produced by a rat bladder carcinoma cell line (804G). Furthermore, in a mixed population of cells, it has been observed previously that spread cells secrete more insulin acutely in response to glucose, compared with cells that remain rounded. These results suggest bi-directional signaling between the islet beta-cell and the extracellular matrix. In the present study, the role of increased intracellular free Ca2+ concentration [Ca2+]i as an intracellular step linking glucose stimulation and beta-cell spreading (inside-out signaling) was investigated. Purified rat beta-cells were attached to this matrix and incubated under various conditions known to affect [Ca2+]i. The effect of glucose on beta-cell spreading was mimicked by 25 mmol/l KCl (which induces calcium influx) and inhibited by diazoxide (which impairs depolarization and calcium entry) and by the L-type Ca2+ channel blocker SR-7037. When a 24-h incubation at 16.7 glucose was followed by 24 h at 2.8 mmol/l, beta-cells that had first spread regained a round phenotype. In the presence of thapsigargin, spreading progressed throughout the experiment, suggesting that capture of calcium by the endoplasmic reticulum is involved in the reversibility of spreading previously induced by glucose. Spreading was still observed in degranulated beta-cells and in botulinum neurotoxin E-expressing beta-cells when exocytosis was prevented. In summary, the results indicate that increased [Ca2+]i is required for the glucose-induced spreading of beta-cells on 804G matrix and that it is not a consequence of exocytotic processes that follow elevation of [Ca2+]i.

Animals↗
PubMed2000

Multiple autocrine factors including an extracellular matrix protein are required for the proliferation and spreading of human colon carcinoma cells in vitro.

The human colon carcinoma cell line LIM1215 proliferates and changes morphology (spread) in a cell density-dependent manner in response to epidermal growth factor (EGF). At high density, production of autocrine transforming growth factor-alpha enables the cells to proliferate and spread in the absence of exogenous EGF or serum. At low cell density (< 1 x 10(4)/cm2) EGF alone fails to elicit a mitogenic or morphological response and requires the presence of conditioned medium (derived from high cell density serum-free culture of the same cells) to exert its effects. This synergy between EGF and LIM1215 conditioned medium was investigated further. Using a low cell density assay and fractionated LIM1215 conditioned medium, we show that EGF-mediated mitogenic and morphological responses are separable. These responses are dependent on the synergistic action of a low molecular weight autocrine survival factor and an extracellular matrix-like spreading factor(s) secreted into the culture medium respectively. We find that under low cell density, serum-free conditions, EGF alone is insufficient to rescue LIM1215 from rapid apoptotic death. Catalase or LIM1215 autocrine survival factor prevent the death of LIM1215 cells and restore their proliferative (but not morphological) response to EGF, suggesting that cell death under these conditions may be the result of oxidative stress. Combination of EGF, partially purified autocrine survival and spreading factors induced proliferation and spreading of low density LIM1215 cells similar to that observed with EGF and unfractionated conditioned medium. GRGDS peptides strongly inhibited the spreading of LIM1215 cells in the presence of EGF and the partially purified autocrine spreading factor, demonstrating that integrin receptors are involved in the spreading process. Comparison of the spreading response of LIM1215 and Colo 526 cells on ASF and various adhesion proteins indicate that ASF is not collagen-I, collagen-IV, fibronectin or vitronectin. Taken together, these results support the concept that the autonomous growth of colon carcinoma cells in vitro is dependent on the synergistic interaction between several autocrine systems.

Animals↗
PubMed1990

Role of actin filaments and microtubules in the spreading of rabbit corneal epithelial cells on the fibronectin matrix.

The migration and spreading of the corneal epithelial cells adjacent to a wound is the first step in successful epithelial resurfacing. To understand the role of actin filaments and microtubules of the cytoskeletal system in the spreading of corneal epithelial cells, we plated rabbit corneal epithelial cells on a fibronectin matrix and studied the effects of cytochalasin B, which inhibits actin filaments assembly, and colchicine, which inhibits microtubules assembly, on the ability of individual cells to spread. Changes in the morphology of actin filaments and microtubules were also studied using immunofluorescent microscopy. The area of spread epithelial cells depended on the concentration of fibronectin used to coat the surface. In spread cells, stress fibers of actin filaments were evenly distributed throughout the cytoplasm, whereas microtubules were observed only at the perinuclear region. The presence of cytochalasin B during the cell attachment and spreading decreased the area of the spread cells more than did colchicine. However, once the epithelial cells were spread on a fibronectin matrix, cytochalasin B and colchicine each decreased the cell area only slightly, and to the same extent. These results indicate that formation of actin filaments is more important than formation of microtubules to the spreading of corneal epithelial cells.

Actins↗
PubMed1990

Surface-activated bovine platelets do not spread, they unfold.

The present study has examined the response of bovine platelets to surface activation and compared it to the reaction of human cells. Human platelets react to surfaces by losing their discoid shape, extending pseudopods, converting to dendritic forms, and finally, spreading into thin films resembling pancakes. Bovine platelets do not spread, they unfold. Surface activation causes them to transform from discs to irregular, flattened shapes resembling dendritic platelets, but they are unable to fill in spaces between pseudopods, a step required for spreading. Bovine platelets lack the surface-connected open canalicular system (OCS), which serves as a reservoir of membrane for human platelet spreading. Its absence may be the major factor in the failure of bovine platelet spreading, but there are other possible factors. Circumferential microtubules are more resistant to disassembly in surface-activated bovine than human cells, and their stability as rings or fractured bundles may limit spreading. Actin filament assembly is similar in human and bovine platelets, but the organization is different. Human platelets form a peripheral weave of actin that expands the membrane between pseudopods. A peripheral weave does not form in surface-activated bovine platelets. The absence of the OCS and differences in cytoskeletal organization in bovine platelets may also affect spreading of the surface membrane. Fibrinogen-gold (Fgn-Au) probes added to spread human platelet move from pseudopods and the cell margin toward the center and concentrate in the OCS. Fgn-Au particles bind to surface-activated bovine cells, but move very little, or not at all. All of these factors may contribute to the inability of bovine platelets to react to surfaces by spreading like human cells, but absence of the OCS appears to be the major cause.

Animals↗
PubMed1993

Covalently immobilized laminin peptide Tyr-Ile-Gly-Ser-Arg (YIGSR) supports cell spreading and co-localization of the 67-kilodalton laminin receptor with alpha-actinin and vinculin.

The laminin-based nonapeptide Cys-Asp-Pro-Gly-Tyr-Ile-Gly-Ser-Arg (CDPGYIGSR) and pentapeptide Tyr-Ile-Gly-Ser-Arg (YIGSR) have been previously demonstrated to support the attachment of several cell types and to competitively bind to the 67-kDa high affinity laminin receptor. Cell attachment, but not spreading, on substrates containing adsorbed CDPGYIGSR or YIGSR was observed. In this report we describe YIGSR-mediated attachment and spreading of a wide variety of cell types. GYIGSRY promoted cell spreading and stress fiber formation when it was covalently immobilized through the amino-terminal Gly residue, used as a spacer arm. Spreading was not observed when adsorbed YIGSR peptide was used. Functionally blocking antiserum directed against the 67-kDa and related laminin-binding proteins blocked human foreskin fibroblast (HFF) spreading, but not attachment, on covalently grafted GYIGSRY substrates. However, functionally blocking antisera directed against the vitronectin receptor, integrin alpha v beta 3, and the fibronectin receptor, integrin alpha 5 beta 1, did not affect HFF spreading on these substrates. When HFFs spread on these substrates, the 67-kDa laminin receptor co-localized with the cytoplasmic proteins alpha-actinin and vinculin into discrete structures. These results suggest that the adhesion ligand YIGSR is solely sufficient for cell spreading when it is conformationally constrained by covalent attachment to a solid substrate, at least when attached via its amino terminus. Furthermore, the role of the 67-kDa laminin receptor in recognition of this ligand and mediating cell attachment is confirmed in this study. This report also provides the first evidence for direct or indirect association of this receptor with vinculin and alpha-actinin when YIGSR-mediated cell spreading occurs.

Actinin↗
PubMed2006

Suppression of EEG gamma activity--an informative measure of spreading depression waves in the neocortex of the conscious rabbit.

Spreading depression can arise spontaneously in convulsions, migraine attacks, vascular lesions, and other pathological brain states. However, the methodological complexity of recording a direct current potential in the neocortex in humans and conscious animals significantly limits studies of the functional consequences of spreading depression. The present report describes a detailed analysis of the EEG dynamics at the moment of development of spreading depression waves and identifies specific signs allowing spreading depression to be recorded without recording changes in the direct current potential. At the moment of arrival of spreading depression, the interhemisphere equilibrium is highly disturbed because of large decreases in high-frequency activity. The time parameters of the dynamics of the gamma-1 and gamma-2 ranges were the most informative features of the development of spreading depression waves. Increases in power in the delta range developed with some delay on the background of a deep inhibition of high-frequency activity and are in essence a consequence of spreading depression. The encephalographic criteria of spreading depression waves identified here can significantly simplify the detection of this phenomenon both in experimental and clinical conditions in a number of pathological brain states.

Animals↗