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At least 253 records · Page 14Linked to original sources
PubMed1989

The spindle-shaped cells in cutaneous Kaposi's sarcoma. Histologic simulators include factor XIIIa dermal dendrocytes.

Kaposi's sarcoma is a neoplasm that develops as multifocal lesions, often involving the skin, characterized by a complex histologic picture including numerous vascular spaces, perivascular and interstitial spindle-shaped cells, and extravasated erythrocytes, lymphocytes, and plasma cells. Using an antibody against factor XIIIa, which identifies dermal dendrocytes, numerous factor XIIIa-positive dermal dendrocytes were detected among the spindle-shaped cells in 12 acquired immune deficiency syndrome (AIDS)-associated, and five non-AIDS-associated Kaposi's sarcoma lesions. The factor XIIIa-positive dermal dendrocytes were also increased in histologic simulators of Kaposi's sarcoma such as dermatofibroma, angiomatoid malignant fibrous histiocytoma, granuloma annulare, and early wound healing, but were absent in keloids. The increased number of dermal dendrocytes, which are often in an angiocentric configuration and which also express CD4, lymphocyte function associated antigen-1 (LFA-1), and Leu M3 in Kaposi's sarcoma, may be important to the angioproliferative response. The results suggested that the spindle-shaped cells that are present in a variety of cutaneous lesions are dermal dendrocytes and belong to the reticuloendothelial system, unlike other mesenchymal cell types such as the endothelial cell. Apparently a diverse array of stimuli, including human immunodeficiency virus type-1 (HIV-1) infection and trauma, can stimulate the accumulation of factor XIIIa expressing dermal dendrocytes in the skin. These cells can then participate in different stages of a variety of cutaneous alterations including Kaposi's sarcoma, dermatofibroma, granuloma annulare, and early wound healing. Thus, the factor XIIIa-positive dermal dendrocyte is a common cellular denominator among diverse clinical entities that share some histologic features.

Acquired Immunodeficiency Syndrome↗
PubMed2005

The Arabidopsis KLUNKER gene controls cell shape changes and encodes the AtSRA1 homolog.

The analysis of a group of seven trichome mutants in Arabidopsis, which all show distorted trichomes along with severe actin defects has revealed insight into the role of the actin cytoskeleton in cell shape control. Four of the corresponding genes encode components of a protein complex, the ARP2/3 complex that stimulates the production of 'fine actin' at active growth sites. In this study, we show that another member of the distorted group, KLUNKER (KLK), encodes the AtSRA1 homolog of Arabidopsis and that klk mutants show a similar range of cell shape defects to those of arp2/3 mutants. In animals, SRA1 regulates the activity of the ARP2/3-regulating WAVE-HSPC300 complex in a Rho-dependent manner. Our findings provide evidence that a Rho/ARP2/3 regulation pathway exists in plants.

Amino Acid Sequence↗
PubMed2005

Shroom regulates epithelial cell shape via the apical positioning of an actomyosin network.

The actin-binding protein Shroom is essential for neural tube morphogenesis in multiple vertebrate organisms, indicating its function is evolutionarily conserved. Shroom facilitates neurulation by regulating the morphology of neurepithelial cells. Shroom localizes to the apical tip of adherens junctions of neural ectoderm cells in vivo and to the apical junctional complex (AJC) in MDCK cells. Induced expression of Shroom in polarized epithelia elicits apical constriction and dramatic reorganization of the apical arrangement and packing of cells without altering apical-basal polarity. These events likely mimic the cell shape changes and cellular movements required for neurulation in vivo. The observed phenotypes depend on the ability of Shroom to alter F-actin distribution and regulate the formation of a previously uncharacterized contractile actomyosin network associated with the AJC. Targeting the C-terminal domain of Shroom to the apical plasma membrane elicits constriction and reorganization of the actomyosin network, indicting that this domain mediates Shroom's activity. In vivo, Shroom-mutant neural epithelia show a marked reduction in apically positioned myosin. Thus, Shroom likely facilitates neural tube closure by regulating cell shape changes via the apical positioning of an actomyosin network in the neurepithelium.

Actins↗
PubMed1984

Effect of extracellular matrix on PC 12 cell shape and dopamine processing.

Substrates of various origins can affect the morphology, growth and functional properties of many cell types. PC 12 cells (a clonal line of rat pheochromocytoma) synthesize, store and secrete dopamine as well as other transmitters. These cells are rounded and loosely attached when cultured on plastic, but flatten and spread extensively when cultured on an extracellular matrix secreted by bovine corneal endothelial cells. We determined that spontaneous dopamine release into culture medium was significantly higher from cells which were flattened on matrix, and that the cellular content of dopamine was less than in cells which were maintained on plastic. The higher levels of medium dopamine in matrix cultures were not due to an increase in cellular attachment or growth as determined by [3H]thymidine incorporation. A variant of PC 12 cells which is flat on plastic showed no change in cell shape or dopamine release when plated on matrix. These experiments suggest that extracellular matrix promotes a change in cell shape and that this change in the physical arrangement of these cells alters their release and storage of dopamine.

Adrenal Gland Neoplasms↗
PubMed1989

Mechanism of endothelial cell shape change in oxidant injury.

Changes in endothelial cell morphology induced by neutrophil-generated hydrogen peroxide (H2O2) may account for the capillary leak of the adult respiratory distress syndrome (ARDS). The relationship of H2O2 effects on the concentration of intracellular Ca2+ [( Ca2+]i) and ATP to changes in microfilaments and microtubules, important determinants of cell shape, was examined. Bovine pulmonary artery endothelial cells were injured over a 2-hr time course with a range of H2O2 doses (0-20 mM). The higher concentrations of H2O2 consistently produced contraction and rounding of greater than 50-75% of cells by 1-2 hr. The range of 1-20 mM H2O2 produced rapid, significant reductions in endothelial ATP levels over the time course of injury. Although there were significant increases in mean endothelial [Ca2+]i in response to 5, 10, and 20 mM H2O2, 1 mM H2O2 did not affect the [Ca2+]i. Fluorescence microscopy revealed that microfilament disruption occurred as ATP levels fell and preceded depolymerization of microtubules which developed after [Ca2+]i approached 1 X 10(-6) M. H2O2 at 1 mM injury caused microfilament disruption but did not depolymerize microtubules. Microfilament disruption occurred without oxidant exposure, when ATP levels were reduced by glucose depletion and mitochondrial inhibition with oligomycin (650 nM). If a Ca2+ ionophore, ionomycin (5 microM), was then added, [Ca2+]i rose to greater than 1 X 10(-6) M, microtubules fragmented and depolymerized, and cell contraction and rounding very similar to that induced by H2O2 occurred. These results suggest that endothelial cell dysfunction and capillary leak in ARDS may be due to H2O2-mediated changes in cellular ATP and [Ca2+]i.

Actin Cytoskeleton↗
PubMed2000

Direct binding of the Na--H exchanger NHE1 to ERM proteins regulates the cortical cytoskeleton and cell shape independently of H(+) translocation.

The association of actin filaments with the plasma membrane maintains cell shape and adhesion. Here, we show that the plasma membrane ion exchanger NHE1 acts as an anchor for actin filaments to control the integrity of the cortical cytoskeleton. This occurs through a previously unrecognized structural link between NHE1 and the actin binding proteins ezrin, radixin, and moesin (ERM). NHE1 and ERM proteins associate directly and colocalize in lamellipodia. Fibroblasts expressing NHE1 with mutations that disrupt ERM binding, but not ion translocation, have impaired organization of focal adhesions and actin stress fibers, and an irregular cell shape. We propose a structural role for NHE1 in regulating the cortical cytoskeleton that is independent of its function as an ion exchanger.

Amino Acid Sequence↗
PubMed1998

Regional differences in cell shape and gap junction expression in rat Achilles tendon: relation to fibrocartilage differentiation.

Tendon cells have complex shapes, with many cell processes and an intimate association with collagen fibre bundles in their extracellular matrix. Where cells and their processes contact one another, they form gap junctions. In the present study, we have examined the distribution of gap junction components in phenotypically different regions of rat Achilles tendon. This tendon contains a prominent enthesial fibrocartilage at its calcaneal attachment and a sesamoid fibrocartilage where it is pressed against the calcaneus just proximal to the attachment. Studies using DiI staining demonstrated typical stellate cell shape in transverse sections of pure tendon, with cells withdrawing their cell processes and rounding up in the fibrocartilaginous zones. Coincident with change in shape, cells stopped expressing the gap junction proteins connexins 32 and 43, with connexin 43 disappearing earlier in the transition than connexin 32. Thus, there are major differences in the ability of cells to communicate with one another in the phenotypically distinct regions of tendon. Individual fibrocartilage cells must sense alterations in the extracellular matrix by cell/matrix interactions, but can only coordinate their behaviour via indirect cytokine and growth factor signalling. The tendon cells have additional possibilities--in addition to the above, they have the potential to communicate direct cytoplasmic signals via gap junctions. The formation of fibrocartilage in tendons occurs because of the presence of compressive as well as tensile forces. It may be that different systems are used to sense and respond to such forces in fibrous and cartilaginous tissues.

Achilles Tendon↗
PubMed1983

Regulation of Cell Shape in Euglena gracilis: I. Involvement of the Biological Clock, Respiration, Photosynthesis, and Cytoskeleton.

The alga Euglena gracilis Z. changes its shape two times per day when grown under the synchronizing effect of a daily light-dark cycle. At the beginning of the light period when photosynthetic capacity is low, the population of cells is largely spherical in shape. The mean cell length of the population increases to a maximum in the middle of the light period when photosynthetic capacity is greatest, and then decreases for the remainder of the 24-hour period. The population becomes spherical by the end of the 24-hour period when the cycle reinitiates. These changes are also observed under constant dim light conditions (up to 72 hours) and are therefore controlled by the biological clock and represent a circadian rhythm in cell shape. In constant dim light, the cell division rhythm is either arrested or slowed considerably, while the cell shape rhythm continues.The involvement of respiratory and photosynthetic pathways in the cell shape changes was investigated with energy pathway inhibitors. Antimycin A and NaN(3) both inhibited the round to long and long to round shape changes, indicating that the respiratory pathways are involved. DCMU and atrazine inhibited the round to long shape change but did not affect the long to round transition, indicating that light-induced electron flow is necessary only for the round to long shape change.The influence of the cell shape changes on the photosynthetic reactions was investigated by altering cell shape with the cytoskeletal inhibitors cytochalasin and colchicine. Both inhibitors blocked the round to long and long to round shape changes. Cytochalasin B was found to have minimal cytotoxic effects on the photosynthetic reactions, but colchicine significantly inhibited light-induced electron flow and the in vivo expression of the photosynthetic rhythm.

Journal Article↗
PubMed2006

The RhoGAP crossveinless-c links trachealess and EGFR signaling to cell shape remodeling in Drosophila tracheal invagination.

A major issue in morphogenesis is to understand how the activity of genes specifying cell fate affects cytoskeletal components that modify cell shape and induce cell movements. Here, we approach this question by investigating how a group of cells from an epithelial sheet initiate invagination to ultimately form the Drosophila tracheal tubes. We describe tracheal cell behavior at invagination and show that it is associated with, and requires, a distinct recruitment of Myosin II to the apical surface of cells at the invaginating edge. We show that this process is achieved by the activity of crossveinless-c, a gene coding for a RhoGAP and whose specific transcriptional activation in the tracheal cells is triggered by both the trachealess patterning gene and the EGF Receptor (EGFR) signaling pathway. Our results identify a developmental pathway linking cell fate genes and cell signaling pathways to intracellular modifications during tracheal cell invagination.

Animals↗
PubMed2005

Small GTPase Rho5 is a functional homologue of Rho1, which controls cell shape and septation in fission yeast.

The small GTPase Rho1 plays an essential role in controlling the organization of the actin cytoskeleton and synthesis of the cell wall in the fission yeast Schizosaccharomyces pombe. Here we studied the role of Rho5 whose primary structure is very similar to that of Rho1. It was found that elevated expression of Rho5 was able to compensate for the lethality of cells lacking Rho1. Rho5 was localized to the ends of interphase cells and the mid-region of mitotic cells. Overexpression of Rho5 caused depolarization of F-actin patches and abnormal formation of the cell wall, as did Rho1. Although rho5(+) was not essential for maintaining the cell shape, rho1 rho5-double null cells showed more severe defects in cell viability than rho1-null cells. Thus, it is likely that Rho5 has an overlapping function with Rho1 in controlling cell growth and division in S. pombe.

Amino Acid Sequence↗
PubMed1969

Microtubules in the formation and development of the primary mesenchyme in Arbacia punctulata. II. An experimental analysis of their role in development and maintenance of cell shape.

TO EXPERIMENTALLY TEST THE SUGGESTION MADE IN THE PRECEDING PAPER THAT THE MICROTUBULES ARE INVOLVED IN CELL SHAPE DEVELOPMENT DURING THE FORMATION AND DIFFERENTIATION OF THE PRIMARY MESENCHYME, WE APPLIED TO THE EMBRYOS TWO TYPES OF AGENTS WHICH AFFECT CYTOPLASMIC MICROTUBULES: (a) colchicine and hydrostatic pressure, which cause the microtubules to disassemble, and (b) D(2)O, which tends to stabilize them. When the first type of agent is applied to sea urchin gastrulae, the development of the primary mesenchyme ceases, the microtubules disappear, and the cells tend to spherulate. With D(2)O development also ceases, but the tubules appear "frozen," and the cell asymmetries persist unaltered. These agents appear to block development by primarily interfering with the sequential disassembly and/or reassembly of microtubules into new patterns. The microtubules, therefore, appear to be influential in the development of cell form. On the other hand through a careful analysis of the action of these agents and others on both intra- and extracellular factors, we concluded that the microtubules do rather little for the maintenance of cell shape in differentiated tissues.

Animals↗
PubMed1998

Role of Rac1 and oxygen radicals in collagenase-1 expression induced by cell shape change.

Integrin-mediated reorganization of cell shape leads to an altered cellular phenotype. Disruption of the actin cytoskeleton, initiated by binding of soluble antibody to alpha5beta1 integrin, led to increased expression of the collagenase-1 gene in rabbit synovial fibroblasts. Activation of the guanosine triphosphate-binding protein Rac1, which was downstream of the integrin, was necessary for this process, and expression of activated Rac1 was sufficient to increase expression of collagenase-1. Rac1 activation generated reactive oxygen species that were essential for nuclear factor kappa B-dependent transcriptional regulation of interleukin-1alpha, which, in an autocrine manner, induced collagenase-1 gene expression. Remodeling of the extracellular matrix and consequent alterations of integrin-mediated adhesion and cytoarchitecture are central to development, wound healing, inflammation, and malignant disease. The resulting activation of Rac1 may lead to altered gene regulation and alterations in cellular morphogenesis, migration, and invasion.

Animals↗
PubMed1992

Cell-shape-associated transcriptional activation of the p52(PAI-1) gene in rat kidney cells.

The microfilament-disrupting agent cytochalasin D (CD) increased (by 10-22-fold) the synthesis de novo and extracellular matrix deposition of plasminogen-activator inhibitor type-1 [p52(PAI-1)] in normal rat kidney (NRK) cells. Transition from a flat to a round phenotype occurred concomitantly with, and may actually precede, p52(PAI-1) induction; both the morphological and p52(PAI-1) responses were dose-dependent. Augmented synthesis became evident between 4 and 5 h of treatment of NRK cells with 100 microM-CD, correlating with a transition from 25 to more than 60% rounded cells. CD-associated increases in p52(PAI-1) mRNA abundance and protein biosynthesis were maximal between 6 and 8 h of continuous CD exposure, declined by 50% thereafter, but remained elevated (by at least 6-21-fold respectively over control values) for 24 h. Changes in p52(PAI-1) mRNA abundance at this 24 h point reflected an approx. 5-fold increase in p52(PAI-1)-gene transcription. These data confirm previous suggestions, based on actinomycin D-sensitivity of the inductive response [Higgins & Ryan (1992) Biochem. J. 284, 433-439], that CD-mediated increases in p52(PAI-1) expression are at least partly due to transcription-level events. Since CD also augments specific cellular responses to growth factors or cytokines, the potential effectiveness of this inducer was evaluated both in the presence and absence of serum growth factors using quiescent NRK cells [a growth state in which p52(PAI-1) is not expressed] as a model system. Induction of p52(PAI-1) synthesis and matrix deposition in CD-stimulated quiescent NRK cells was as efficient under growth-factor-deficient conditions as when CD was added simultaneously with serum. CD alone is thus a complete inducer of p52(PAI-1) expression in NRK cells, an observation that supports the contention that cell shape is an important regulatory element in p52(PAI-1)-gene control.

Animals↗
PubMed1997

Regulation of endothelin-1 gene expression by cell shape and the microfilament network in vascular endothelium.

Endothelial synthesis and release of endothelin-1 (ET-1) are exquisitely regulated by external shear and strain. We tested the hypothesis that manipulation of endothelial cell shape can regulate ET-1 gene expression. Treatment of bovine aortic endothelial cell (BAEC) monolayers with cytochalasin D disrupted F-actin and induced cell retraction and rounding, in parallel with time- and dose-dependent specific decreases in ET-1 mRNA levels. Treatments with forskolin, phorbol 12-myristate 13-acetate, staurosporine, and genistein also induced cell shape change and decreased F-actin staining and ET-1 mRNA levels. BAEC plated onto nonadhesive petri dishes coated with decreasing concentrations of synthetic RGD polymer showed RGD dose-dependent decreases in cell spreading and in F-actin microfilament elaboration. These changes were specifically accompanied by decreases in ET-1 peptide secretion (60%) and, via posttranscriptional mechanisms, ET-1 mRNA (94%) and were not due to decreased cell-cell contact. We conclude that the shape and microfilament network of endothelial cells are potent posttranscriptional regulators of ET-1 gene expression.

Actin Cytoskeleton↗
PubMed1985

Oscillations in cell shape and size during locomotion and in contractile activities of Physarum polycephalum, Dictyostelium discoideum, Amoeba proteus and macrophages.

Changes in cell shape and size were measured during locomotion, together with the motive force of the protoplasmic streaming, in various amoeboid cells in different stages of their life cycle, and under various environmental conditions. The variations in these measurements with time were examined by Fourier spectral analysis. Notwithstanding a change in cell type in the life cycle of P. polycephalum, myxamoebae and tiny plasmodia showed a similar time pattern of locomotion, exhibiting oscillations having a mixture of several periods. A regular oscillation with protoplasmic streaming appeared in the plasmodium only above a critical cell size. D. discoideum amoebae oscillated with two periods of a few minutes in preaggregation stage, but with a period of 10 min in aggregation stage, the latter being induced by cAMP. Macrophages and A. proteus also oscillated with periods of a few minutes. Periods of all these oscillations were prolonged severalfold by respiratory inhibition with NaCN, but were unaffected by glycolytic inhibition with 2-deoxyglucose. Cell fragments of A. proteus containing fewer granules oscillated more slowly and with a larger amplitude than those containing more granules. Among the granules, the nucleus was excluded as a possible modifier of the oscillation. The oscillation in Physarum plasmodium was reversibly suppressed by combining respiratory and ATPase inhibitions in mitochondria with NaCN and oligomycin, intracellular ATP concentration being kept at an appropriate level. The present results show that amoeboid motility, as well as cell shape, is oscillatory and that mitochondria are involved in time keeping.

Adenosine Triphosphate↗
PubMed1980

Effect of prostaglandin E1 on the level of cAMP in bone marrow macrophages. Inhibition of phagocytosis and cell shape changes.

The effect of prostaglandins E1 (PGE1) and F2 alpha (PGF 2 alpha) on levels of cAMP, cell shape and phagocytosis of zymosan were examined. The addition of 10(-6) M PGE1 induced an immediate rise in the level of cAMP which fell again after 2.5 min. Phagocytosis was inhibited only after 60 min. of drug treatment. PGF 2 alpha did not show this effect. Neither db-cAMP or papaverine showed a similar effect on phagocytosis and cell shape to that produced by PGE1 treatment. Therefore, we conclude, that PGE1 does at least not exclusively act by changing cAMP levels, but rather directly influences cell membrane functions.

Animals↗
PubMed1979

Asymmetric manipulation of the membrane lipid bilayer of intact human erythrocytes with phospholipase A, C, or D induces a change in cell shape.

Changes in the membrane morphology and phospholipid content of human erythrocytes were determined after incubation of intact cells with each of various exogeneous phospholipases (PLases). PLase A2 from Naja naja or bee venom induced crenation of the cells in parallel with hydrolysis of the membrane phosphatidylcholine (PC). This crenated cell shape was reversed to a biconcave disc or cup-like form by a further treatment with lysophospholipase. In contrast, bacterial PLase C from Clostridium perfringens and Pseudomonas aureofaciens or fungal PLase D from Streptomyces chromofuscus induced invagination of the cells in parallel with hydrolysis of the PC. The action of the latter group of PLases on the membrane morphology was counteracted by PLase A2, and vice versa. Thus, participation of the membrane lipid bilayer in the induction of membrane conformational change and hence cell shape change was demonstrated.

Erythrocyte Membrane↗
PubMed1992

The effects of receptor density and cell shape on epidermal growth factor binding.

In this paper we describe the effects of receptor density and cell shape on the binding of epidermal growth factor (EGF) to its receptor. Association kinetics of EGF binding to cells with a high receptor density was done using A431 cells. The association rate of EGF binding was apparently independent of the EGF concentration, most likely due to diffusion limited EGF binding as result of high receptor density. The effect of receptor density on EGF association rate was examined by reducing the number of functional EGF receptors on A431 cells. Preincubation of the cells with a monoclonal antibody directed against the EGF receptor and isolation of the cytoskeletons of A431 cells which both leaves only EGF binding to high affinity receptors revealed an EGF concentration dependent association rate. These results were confirmed in HeLa cells with 40 times less receptor numbers than A431 cells demonstrating the effect of receptor density on EGF binding. The influence of shape of the cell on EGF binding was examined by comparing the EGF association to monolayer cells with that of suspension cells. EGF association to suspended A431 cells was EGF concentration dependent. In conclusion we have shown that binding of EGF to A431 cells is dependent not only on the intrinsic rate constants but in addition on both receptor numbers per cell and the shape of cells. These results are in agreement with the hypothesis that EGF binding can be restricted by limited diffusion.

Antibodies, Monoclonal↗