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PubMed1990

The role of actin in changes of cell shape and steroidogenesis in mouse Y-1 cells stimulated by ACTH--immunocytochemical studies.

We investigated the immunocytochemical localization of two kinds of representative cytoskeletal proteins (tubulin and actin) and the morphology of Y-1 mouse adrenal tumor cells under ACTH stimulation at the light and electron microscopic levels. After ACTH stimulation, Y-1 cells showed the rounding-up phenomenon and increased steroidogenesis. Meanwhile, actin was accumulated near the cell membrane and formed filaments. Electron microscopically, stress fibers disappeared with ACTH administration. However, changes in the tubulin localization (main element of the microtubules) were not conspicuous. Cytochalasin B which blocks formation of actin filaments induced rounding-up of Y-1 cells and inhibited increases of steroid synthesis induced by ACTH. Colchicine caused disappearance of the microtubule-organizing center, but the shape of Y-1 cells was not changed. These results suggested that actin-filaments may be the main filament involved in the changes of cell shape and the increased steroidogenesis induced by ACTH.

Actins↗
PubMed1997

Transforming growth factor-beta1 induces a mesenchyme-like cell shape without epithelial polarization in thyrocytes and inhibits thyroid folliculogenesis in collagen gel culture.

Transforming growth factor-beta1 (TGFbeta1) induces a mesenchyme-like cell shape in some epithelial cell types. To clarify the role of TGFbeta1 in the morphological regulation of thyrocytes, we performed collagen gel culture of porcine thyrocytes with serum-free medium. TGFbeta1-nontreated cells organized follicles. In contrast, the cells treated with 10 ng/ml TGFbeta1 became spindle shaped, i.e. they resembled mesenchymal fibroblasts, and did not form follicles. To characterize the spindle-shaped cells, we examined the fine structures and expression of thyroglobulin (Tg) and cytoskeletal proteins using electron microscopy, immunohistochemistry, and immunoblotting. TGFbeta1-nontreated cells had microvilli at the apical side facing follicle lumen and had basal lamina at the basal side in contact with collagen gel. TGFbeta1-treated cells showed both microvilli and basal lamina at the basal side. TGFbeta1-nontreated cells expressed Tg, whereas TGFbeta1-treated cells showed no expression. TGFbeta1-nontreated cells barely expressed vimentin, but they expressed enough cytokeratin. TGFbeta1-treated cells extensively displayed vimentin along with the change in shape to become spindle-like and retained a decreased expression of cytokeratin. TSH (10 mU/ml) did not essentially influence any TGFbeta1 effects on the cells. These results indicate that TGFbeta1 induces a mesenchyme-like cell shape accompanied by cytoskeletal molecular change and the loss of both epithelial polarization and a function in thyrocytes, and that it results in inhibiting thyroid folliculogenesis with or without TSH.

Animals↗
PubMed2005

Two independent spiral structures control cell shape in Caulobacter.

The actin homolog MreB contributes to bacterial cell shape. Here, we explore the role of the coexpressed MreC protein in Caulobacter and show that it forms a periplasmic spiral that is out of phase with the cytoplasmic MreB spiral. Both mreB and mreC are essential, and depletion of either protein results in a similar cell shape defect. MreB forms dynamic spirals in MreC-depleted cells, and MreC localizes helically in the presence of the MreB-inhibitor A22, indicating that each protein can form a spiral independently of the other. We show that the peptidoglycan transpeptidase Pbp2 also forms a helical pattern that partially colocalizes with MreC but not MreB. Perturbing either MreB (with A22) or MreC (with depletion) causes GFP-Pbp2 to mislocalize to the division plane, indicating that each is necessary but not sufficient to generate a helical Pbp2 pattern. We show that it is the division process that draws Pbp2 to midcell in the absence of MreB's regulation, because cells depleted of the tubulin homolog FtsZ maintain a helical Pbp2 localization in the presence of A22. By developing and employing a previously uncharacterized computational method for quantitating shape variance, we find that a FtsZ depletion can also partially rescue the A22-induced shape deformation. We conclude that MreB and MreC form spatially distinct and independently localized spirals and propose that MreB inhibits division plane localization of Pbp2, whereas MreC promotes lengthwise localization of Pbp2; together these two mechanism ensure a helical localization of Pbp2 and, thereby, the maintenance of proper cell morphology in Caulobacter.

Bacterial Proteins↗
PubMed2003

Cyclic AMP-dependent cell shape changes induced by mechanical forces.

Biomaterials used in some biomedical devices are exposed to flow of physiological fluids. The flow-induced forces may influence the morphological and the biochemical responses of adhering cells. The objective of this work is to examine the capacity of a mechanical stress to cause changes in cell/substratum and cell/cell interactions via the second messenger cAMP pathway (cyclic Adenosine Monophosphate). Cyclic AMP is known to modulate cell shape, cell adhesion and intercellular communication in static conditions. A specially designed flow chamber was used to analyze the responses of mouse 3T3 fibroblasts spread on biocompatible substrata and submitted to controlled shear stresses. A 1.1-Pa shear stress induced: cell rounding, disruption of vitronectin receptors clusters and clustering of connexins 43 at cell-cell apposition points. These cell responses were cAMP-dependent. These investigations should help provide a better understanding of the early biochemical events triggered by mechanical forces.

Animals↗
PubMed1992

Mechanisms of cell shape change: the cytomechanics of cellular response to chemical environment and mechanical loading.

Processes such as cell locomotion and morphogenesis depend on both the generation of force by cytoskeletal elements and the response of the cell to the resulting mechanical loads. Many widely accepted theoretical models of processes involving cell shape change are based on untested hypotheses about the interaction of these two components of cell shape change. I have quantified the mechanical responses of cytoplasm to various chemical environments and mechanical loading regimes to understand better the mechanisms of cell shape change and to address the validity of these models. Measurements of cell mechanical properties were made with strands of cytoplasm submerged in media containing detergent to permeabilize the plasma membrane, thus allowing control over intracellular milieu. Experiments were performed with equipment that generated sinusoidally varying length changes of isolated strands of cytoplasm from Physarum polycephalum. Results indicate that stiffness, elasticity, and viscosity of cytoplasm all increase with increasing concentration of Ca2+, Mg2+, and ATP, and decrease with increasing magnitude and rate of deformation. These results specifically challenge assumptions underlying mathematical models of morphogenetic events such as epithelial folding and cell division, and further suggest that gelation may depend on both actin cross-linking and actin polymerization.

Actins↗
PubMed2005

The cell-shape protein MreC interacts with extracytoplasmic proteins including cell wall assembly complexes in Caulobacter crescentus.

The bacterial actin homolog, MreB, forms helical cables within the cell that are required for maintenance of a rod shape. These helical structures are thought to be involved in the spatial organization of cell wall (peptidoglycan) synthesizing complexes of penicillin-binding proteins (PBPs). Here, we examined the role of the MreC cell shape protein in this process in Caulobacter crescentus. Subcellular fractionation experiments showed that MreC is a periplasmic protein and, as assayed by immunofluorescence microscopy, adopted helical or banded patterns along the cell length reminiscent of those formed by MreB and PBP2. The pattern of MreC and PBP2 localization remained when MreB cables were disrupted by treatment with the inhibitor A22. However, long-term absence of MreB led to cell shape changes and an eventual loss of MreC localization, suggesting that an independent structure, perhaps an intact peptidoglycan layer, contributes to the MreC localization pattern. Using affinity chromatography with MreC covalently bound to Sepharose, we isolated several PBPs from cell extracts that eluted from the column as heterogeneous complexes. In this same experiment, using mass spectrometry-based protein identification, we identified several outer membrane proteins, including TonB-dependent receptor transport proteins, that interacted with MreC. Imaging live cells containing fusions of these outer membrane proteins to green fluorescent protein showed that they adopted a subcellular localization pattern that was similar to that of MreC. These results suggest that MreC may function in the spatial organization of PBPs as well as other proteins that lie outside the cytoplasmic membrane.

Bacterial Proteins↗
PubMed1988

Loss of metastatic responsiveness to cell shape modulation in a newly characterized B16 melanoma adhesive cell variant.

Repeated selection of an adherent subpopulation from B16-F1 melanoma cells growing in suspension culture on poly(hydroxyethylmethacrylate) [poly(HEMA)] coated plates resulted in the isolation of an adherent variant designated B16-A10. B16-A10 cells are more adherent to poly(hydroxyethylmethacrylate) coated plates than are B16-F1 cells and express an organized actin structure characteristic of highly adherent low metastatic cells as opposed to the poor cytoskeletal organization of B16-F1 cells. Upon growth in suspension, B16-A10 cells do not acquire the enhanced metastatic capability characteristic of B16-F1 cells and they express similar lung colonizing ability irrespective of the culture conditions. The increased metastatic ability of B16-F1 cells in suspension culture has previously been associated with the decreased accessibility of surface proteins to lactoperoxidase catalyzed iodination and with the increased expression of sialylated peanut agglutinin-binding oligosaccharides on these proteins. B16-A10 cells which show no cell shape induced increase in metastatic ability do not undergo alteration in either of these two properties in suspension culture. The absence of these two phenomena on B16-A10 cells grown in suspension indicates that they are interrelated and involved in the increased metastatic ability of B16-F1 cells grown in suspension.

Animals↗
PubMed1999

Resolution of the paradox of red cell shape changes in low and high pH.

The molecular basis of cell shape regulation in acidic pH was investigated in human erythrocytes. Intact erythrocytes maintain normal shape in the cell pH range 6.3-7.9, but invaginate at lower pH values. However, consistent with predicted pH-dependent changes in the erythrocyte membrane skeleton, isolated erythrocyte membranes evaginate in acidic pH. Moreover, intact cells evaginate at pH greater than 7.9, but isolated membranes invaginate in this condition. Labeling with the hydrophobic, photoactivatable probe 5-[125I]iodonaphthyl-1-azide demonstrated pH-dependent hydrophobic insertion of an amphitropic protein into membranes of intact cells but not into isolated membranes. Based on molecular weight and on reconstitution experiments using stripped inside-out vesicles, the most likely candidate for the variably labeled protein is glyceraldehyde-3-phosphate dehydrogenase. Resealing of isolated membranes reconstituted both the shape changes and the hydrophobic labeling profile seen in intact cells. This observation appears to resolve the paradox of the contradictory pH dependence of shape changes of intact cells and isolated membranes. In intact erythrocytes, the demonstrated protein-membrane interaction would oppose pH-dependent shape effects of the spectrin membrane skeleton, stabilizing cell shape in moderately abnormal pH. Stabilization of erythrocyte shape in moderately acidic pH may prevent inappropriate red cell destruction in the spleen.

Azides↗
PubMed2003

The effects of continuous and discontinuous groove edges on cell shape and alignment.

Nanofabricated model surfaces and digital image analysis of cell shape were used to address the importance of a continuous sharp edge in the alignment of cells to shallow surface grooves. The grooved model surfaces had either continuous or discontinuous edges of various depths (40-400 nm) but identical surface chemistry and groove/ridge dimensions (15 microm wide). Epithelial cells were cultured on the model surfaces for 10 and 24 h. Fluorescence microscopy combined with image analysis were used to quantify cell area and alignment and to make cell shape classifications of individual cells. The degrees of alignment of cells and the percentages of elongated cell classes increased with groove depth on samples with continuous grooves. Two main differences, with regard to cell response, were observed between the continuous and discontinuous grooved surfaces. First, significantly fewer cells aligned to surface grooves with discontinuous edges than to grooves with continuous edges. Second, there were lower percentages of the elongated cell classes on discontinuous grooves than on continuous ones. We concluded that grooved surfaces with continuous edges are more potent in aligning and inducing elongated cells. The results from the present study suggest that a mechanism of alignment involving orientation along a continuous edge is likely.

Animals↗
PubMed1981

Lateral organization of membranes and cell shapes.

The relations among membrane structure, mechanical properties, and cell shape have been investigated. The fluid mosaic membrane models used contains several components that move freely in the membrane plane. These components interact with each other and determine properties of the membrane such as curvature and elasticity. A free energy equation is postulated for such a multicomponent membrane and the condition of free energy minimum is used to obtain differential equations relating the distribution of membrane components and the local membrane curvature. The force that moves membrane components along the membrane in a variable curvature field is calculated. A change in the intramembrane interactions can bring about phase separation or particle clustering. This, in turn, may strongly affect the local curvature. The numerical solution of the set of equations for the two dimensional case allows determination of the cell shape and the component distribution along the membrane. The model has been applied to describe certain erythrocytes shape transformations.

Animals↗
PubMedDate not supplied

Modulation of hepatocyte function by changing the cell shape in primary culture.

To study the role of cell shape in control of hepatocyte function, we have developed a system that can quantitatively control the spreading of cultured rat hepatocytes using poly[2-hydroxyethyl methacrylate]. When hepatocytes were cultured in a dish coated with high concentration of poly[2-hydroxyethyl methacrylate] solution, formation of stress fibers were suppressed and they continued to have a compact shape. In the compact-shaped hepatocytes, the ability to induce tyrosine aminotransferase with dexamethasone remained high for longer periods of time, as compared to the hepatocytes that spread following culture in the polystyrene dish. Conversely, the hepatocytes showed more active DNA synthesis when they assumed a flat shape as a result of spreading. When the hepatocytes that had spread following long-term culture in the polystyrene dishes were treated with cytochalasin to induce depolymerization of F-actin, the ability of the cells to induce tyrosine aminotransferase upon stimulation with dexamethasone improved markedly. This effect was not altered by treatment with actinomycin D but was completely suppressed by cycloheximide, suggesting that microfilaments are involved in the post-transcriptional process of tyrosine aminotransferase induction. Thus, there is a possibility that F-actin rather than cell shape might regulate cellular function in primary cultured hepatocytes.

Actins↗
PubMed1992

Electrical method for detection of endothelial cell shape change in real time: assessment of endothelial barrier function.

We have developed an electrical method to study endothelial cell shape changes in real time in order to examine the mechanisms of alterations in the endothelial barrier function. Endothelial shape changes were quantified by using a monolayer of endothelial cells grown on a small (10(-3) cm2) evaporated gold electrode and measuring the changes in electrical impedance. Bovine pulmonary microvessel endothelial cells and bovine pulmonary artery endothelial cells were used to study the effects of alpha-thrombin on cell-shape dynamics by the impedance measurement. alpha-Thrombin produced a dose-dependent decrease in impedance that occurred within 0.5 min in both cell types, indicative of retraction of endothelial cells and widening of interendothelial junctions because of "rounding up" of the cells. The alpha-thrombin-induced decrease in impedance persisted for approximately 2 hr, after which the value recovered to basal levels. Pretreatment of endothelial cells with the protein kinase C inhibitor, calphostin C, or with 8-bromoadenosine 3',5'-cyclic monophosphate prevented the decreased impedance, suggesting that the endothelial cell change is modulated by activation of second-messenger pathways. The alpha-thrombin-induced decrease in impedance was in agreement with the previously observed increases in transendothelial albumin permeability and evidence of formation of intercellular gaps after alpha-thrombin challenge. The impedance measurement may be a valuable in vitro method for the assessment of mechanisms of decreased endothelial barrier function occurring with inflammatory mediators. Since the rapidly occurring changes in endothelial cell shape in response to mediators such as thrombin are mediated activation of second-messenger pathways, the ability to monitor endothelial cell dynamics in real time may provide insights into the signal-transduction events mediating the increased endothelial permeability.

Animals↗
PubMed2003

Cell shape and gene expression in human intervertebral disc cells: in vitro tissue engineering studies.

The objective of the present study was to examine the relation between gene expression and the shape of human intervertebral disc cells cultured in vitro in three-dimensional (3D) scaffolds. Disc cells from 19 subjects were seeded into either a collagen sponge or collagen gel and cultured for 10 days. In situ hybridization was performed on serial sections of paraffin embedded specimens and assessed for expression of selected genes important for extracellular matrix formation: Types I and II collagen, aggrecan and chondroitin-6 sulfotransferase. Rounded cells grown in collagen gel showed expression of Types I and II collagen, aggrecan and chondroitin-6 sulfotransferase; expression of these genes was absent in spindle shaped cells. Cells in the collagen sponge that lay on the sponge margin were frequently spindle shaped; these cells expressed type I collagen, but not type II collagen, aggrecan or chondroitin-6 sulfotransferase. Results presented here provide novel data concerning disc cell gene expression with collagen 3D constructs. This information is useful for future tissue engineering studies that have the challenging goal of selectively modulating gene expression.

Adult↗
PubMed1993

Microtubule-dependent control of cell shape and pseudopodial activity is inhibited by the antibody to kinesin motor domain.

One of the major functions of cytoplasmic microtubules is their involvement in maintenance of asymmetric cell shape. Microtubules were considered to perform this function working as rigid structural elements. At the same time, microtubules play a critical role in intracellular organelle transport, and this fact raises the possibility that the involvement of microtubules in maintenance of cell shape may be mediated by directed transport of certain cellular components to a limited area of the cell surface (e.g., to the leading edge) rather than by their functioning as a mechanical support. To test this hypothesis we microinjected cultured human fibroblasts with the antibody (called HD antibody) raised against kinesin motor domain highly conserved among the different members of kinesin superfamily. As was shown before this antibody inhibits kinesin-dependent microtubule gliding in vitro and interferes with a number of microtubule-dependent transport processes in living cells. Preimmune IgG fraction was used for control experiments. Injections of fibroblasts with HD antibody but not with preimmune IgG significantly reduced their asymmetry, resulting in loss of long processes and elongated cell shape. In addition, antibody injection suppressed pseudopodial activity at the leading edge of fibroblasts moving into an experimentally made wound. Analysis of membrane organelle distribution showed that kinesin antibody induced clustering of mitochondria in perinuclear region and their withdrawal from peripheral parts of the cytoplasm. HD antibody does not affect either density or distribution of cytoplasmic microtubules. The results of our experiments show that many changes of phenotype induced in cells by microtubule-depolymerizing agents can be mimicked by the inhibition of motor proteins, and therefore microtubule functions in maintaining of the cell shape and polarity are mediated by motor proteins rather than by being provided by rigidity of tubulin polymer itself.

Animals↗
PubMed1992

Epithelial morphogenesis in developing Artemia: the role of cell replication, cell shape change, and the cytoskeleton.

The roles of cell replication and shape change as morphogenetic forces in epithelial invagination were examined in instar II Artemia. The epidermal cells underwent a fixed pattern of cell division during the first 5 hr of instar II. Greater cell replication in the thoracopod bud (ThB) than in the arthrodial membrane (AM) region resulted in a higher density of epidermal cells in the ThB region (differential cell density). The ratio of cell density (AM/ThB) declined from 1.0 to less than 0.80 by Hour 2 of instar II. Invagination of the AM occurred during Hour 4 when the AM/ThB reached 0.75. A 2-hr pulse with 5'-fluorodeoxyuridine (FudR) during instar I delayed completion of the cell replication pattern and development of transverse cell files in the ThB region for a period equal to the length of the exposure. The delay in the cell division program resulted in a cell density ratio of 0.93 at Hour 4, a value normally observed in Hour 2 larvae, and evagination of the epidermis did not occur at apolysis (Hour 4). The FudR treatment did not perturb the cytoskeleton or the initial steps in cell shape change and the larvae formed small segments during instar III. Cell shape change within the AM began during Hour 4 as this region became significantly thinner than the neighboring ThB region (thickness ratio, AM/ThB = 0.77). Before apolysis the AM cells became wedge shaped, a change which occurred when the basal region of the cell enlarged. The microtubules and microfilaments were reorganized from the apical cytoplasm to the lateral border of apposing AM cells. Following apolysis (Late Hour 4) shape change was completed as the cells attained a thin spindle form, with microtubule- and microfilament-rich filopodial extensions which overlapped adjacent AM cells. As contact with ThB cells shifted from lateral to apicolateral, the AM cells formed the innermost edge of the invagination. Microtubules in the differentiating AM cells contained tyrosinated, detyrosinated, and acetylated alpha-tubulin isoforms. Treatment with nocodazole, colchicine, taxol, or cytochalasin B blocked AM cell shape change and inhibited segmentation, but did not affect the mitotic pattern or differential cell density. We conclude that the specific pattern of cell division led to differential cell density which, along with AM cell shape change, established the conditions necessary to achieve epidermal evagination.

Actin Cytoskeleton↗
PubMed1999

Effect of cell shape on dielectric behavior of fission yeast.

In order to study the effect of cell shape on dielectric behavior of cell suspensions, a temperature sensitive cell division cycle mutant cdc25-22, of Schizosaccharomyces pombe was used, whose cell length was varied by cultivating at the restrictive temperature. The dielectric dispersion of the cells in suspension was mainly composed of two subdispersions. The low-frequency subdispersion depended on the cell length, whereas the high-frequency subdispersion was independent of it. The cell shape effect was qualitatively simulated by an ellipsoidal cell model.

Cell Size↗
PubMed1993

Cell shape changes induced by sulphate in the Cloudman mouse melanoma cell line.

The mechanism of cell shape changes and haematogenous translocations (metastases) in mouse malignant melanoma cells induced by phorbol esters and protein kinase C (PKC) is reported as adhesion "downregulation", exocytosis and motility. However, PKC activation also produces intracellular alkalinization, a causal factor in plasma membrane internalization, cell rounding and detachment that does not necessarily implicate specific cell adhesion downregulation. We show here that Cloudman mouse malignant melanoma cells can be induced to round up and detach with concomitant intracellular alkalinization by simple inorganic sulphate treatment, thereby suggesting an alternative explanation to the reported phenomena.

Animals↗
PubMed1998

Interactions of signaling pathways in ACTH (1-24)-induced cell shape changes in invertebrate immunocytes.

ACTH (1-24) induces cell shape changes in the immunocytes of the bivalve mollusc, Mytilus galloprovincialis. Using computer-assisted microscopic image analysis, we have found that the G protein antagonist suramin sodium, the adenylate cyclase inhibitor 2',5'-dideoxyadenosine, and the protein kinase inhibitor staurosporine inhibit this effect. The highly specific inhibitors H-89 (for protein kinase A) and calphostin C (for protein kinase C) only inhibited partially the morphological alterations. In contrast, the simultaneous action of H-89 and calphostin C completely blocked these changes. The above findings indicate that ACTH (1-24) induces cell shape changes in molluscan immunocytes via adenylate cyclase/cAMP/protein kinase A pathway, as well as the activation of protein kinase C.

Adenylyl Cyclase Inhibitors↗