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At least 649 records · Page 36Linked to original sources
PubMed2002

50 Hz magnetic fields of varying flux intensity affect cell shape changes in invertebrate immunocytes: the role of potassium ion channels.

The effect induced by exposure to 50 Hz magnetic fields (MFs) in immunocytes from the mussel Mytilus galloprovincialis is evaluated. The whole animal was exposed for 15 and 30 min to MF intensities ranging from 200 to 1,000 microT. The changes in the cellular shape of immunocytes, expressed as shape factor (SF), were studied at different times after addition of the chemotacting substance N-formyl-Meth-Leu-Phe (fMLP). Results show that MFs provoke differing delays in fMLP-induced cellular shape changes: 200 microT are ineffective, while levels from 300 microT upwards cause a significant increase in immunocyte SF values compared to controls. Reactivation of the cells is possible up to an intensity of 600 microT. The use of PCO 400, an opener of ATP-sensitive K+ channels, shows that potassium channels are involved in the effect of MFs on M. galloprovincialis immunocytes.

Analysis of Variance↗
PubMed1981

Control of cell shape by calcium in the euglenophyceae.

The euglenoid flagellates are able to change their shape rapidly in response to a variety of stimuli, or sometimes spontaneously. Two extremes of shape can be identified: the "relaxed" form is cylindrical; the contracted form is a somewhat distorted disc. These 2 forms can be interconverted by treatments that alter the Ca2+ concentration of the entire cell. The level of Ca2+ is believed to be normally controlled by a system of calcium-accumulating membranes, identified in Astasia longa by the technique of calcium oxalate precipitation. The system forms a set of parallel tubes of endoplasmic reticulum, one of which lies immediately below each of the ridges of the pellicle. The individual ridges, each with its associated reticulum, microtubules and other elements are suggested to be independent motor units. Local activation of a small number of these units by Ca2+ is made possible by the arrangement of Ca2+ -sequestering reticulum, producing the characteristic squirming euglenoid movement. Uniform activation or suppression of all units produces the 2 extremes of shape. The pellicle of A. longa with its associated microtubules has been purified and shown to contain a Ca2+ -binding site and ATPase activity.

Adenosine Triphosphatases↗
PubMed1996

Smooth muscle alpha-actin downregulation in cultured chick aortic smooth muscle and neural crest cells is associated with altered cell shape.

A modified CXL retrovirus was used to clone an antisense smooth muscle alpha-actin ribozyme sequence adjacent to the reporter lacZ sequence. The virus was applied to downregulate alpha-actin expression in cultured smooth muscle cells obtained from chicken aortic arch and cultured neural crest cells. After infection with the ribozyme-containing CXL retrovirus both the smooth muscle and neural crest cells showed beta-galactosidase activity accompanied by a reduction of smooth muscle alpha-actin-positive fibers. Double staining of beta-galactosidase and smooth muscle alpha-actin using immunohistochemistry revealed that single cells infected with the CXL/ribozyme showed little to no smooth muscle alpha-actin protein. The absence of smooth muscle alpha-actin was associated with a distinct change in cellular morphology of the cultured cells, suggesting that expression of smooth muscle alpha-actin in cultured neural crest cells may be associated with cytoskeletal elements rather than vascular smooth muscle phenotype.

Actins↗
PubMed1987

Influence of cell shape and adhesiveness on stratification and terminal differentiation of human keratinocytes in culture.

Human epidermal keratinocytes can be grown in culture under conditions in which they assemble a tissue with the same basic organization as normal epidermis. The cells stratify, mitosis is restricted to the basal layer and terminal differentiation occurs as the cells move through the suprabasal layers. Keratinocytes do not have to leave the basal layer in order to undergo terminal differentiation, but the two processes are normally linked, because during terminal differentiation the adhesive affinity of keratinocytes for the culture substratum and for other keratinocytes is reduced. Down-regulation of synthesis of basement membrane components and their receptors may provide the molecular basis for the reduction in cell-substratum adhesiveness. However, the molecules that mediate changes in cohesiveness have not yet been identified. Restriction of substratum contact, so that cells are prevented from spreading, appears to be one signal that induces keratinocytes to stop dividing and undergo terminal differentiation.

Cell Adhesion↗
PubMed1982

Interaction of cholesterol and lysophosphatidylcholine in determining red cell shape.

The effect of lysolecithin on the shape of human erythrocytes of varied cholesterol content was examined by scanning electron microscopy. Under the conditions of these experiments, all of the [14C]lysolecithin incubated with cells was shown to be located in the external membrane leaflet. The membrane lysolecithin required to induce echinocytosis (spiculation) in normal cells (0.8 mol cholesterol/mol phospholipid) was approximately 0.08-0.10 mumol/10(10) cells, which contributed 1.6-2.0 micrometer 2 or 1% of the cell surface area. This value is consistent with the premise that echinocytosis was caused by a slight differential expansion of the outer surface of the bilayer. The lysolecithin required for echinocytosis decreased as the membrane cholesterol content increased; from 0.14 mumol/10(10) cells at 0.5 mol cholesterol/mol phospholipid to 0.03 mumol/10(10) cells at 1.4 mol cholesterol/mol phospholipid. These data were interpreted in terms of a bilayer couple mechanism. Assuming that the two amphipaths acted additively, the amount of lysolecithin required to induce echinocytosis was used to estimate the partition of cholesterol between the two leaflets of the red cell membrane. A value of about 51:49% in favor of the outer leaflet was found at all cholesterol levels.

Cholesterol↗
PubMed1993

In vitro organotin administration alters guinea pig cochlear outer hair cell shape and viability.

Trimethyltin (TMT) and triethyltin (TET) disrupt auditory function at doses far below those shown to be neurotoxic. In vivo studies suggest that the initial effect of TMT on hearing occurs at the inner hair cell/spiral ganglion cell synapse, while later, the outer hair cell (OHC) undergoes structural and functional damage. TET produces acute effects upon afferent neurotransmission similar to those observed following TMT, but TET's effects on OHC structure and function have not been examined. OHCs are motile elements within the cochlea, believed to modulate the sensitivity and tuning within the inner ear. Changes in OHC length may alter hearing function, and length changes have been reported following exposure to various ototoxic agents in vitro. In the present study, 77 OHCs from 45 pigmented male guinea pigs were isolated in primary culture and exposed for 90 min to concentrations between 30 microM and 1.0 mM of TMT or TET and then to bathing medium for 30 min to remove the toxicant. Significant shortening of the OHC cell body occurred at all doses to both organotins, with a mean reduction in length of 15.1 and 20.2% for 1.0 mM TMT and TET, respectively, at the end of testing; control cells were only 3.4% shorter at the end of 90 min of perfusion with bathing medium. The effect of organotin exposure on OHC volume was not consistently related to either TMT or TET concentration or altered cell length. In addition, disruption of the plasma membrane characterized by bleb formation, the forceful ejection of cytoplasm, or bursting was seen in 80% of cells exposed to 1.0 mM TET, although not TMT; lower concentrations of both organotins disrupted the cell membrane in 10-30% of cells. Membrane rupture was not reliably associated with either increased cell volume or decreased length, implicating a weakening of the plasma membrane or cortical lattice as the basis for this effect. Consistent with the irreversible structural weakening of the lateral wall, resorption of organotin-induced cytoplasmic blebs was never evidenced. Qualitatively, subcellular elements in the central core of many organotin-treated OHCs appeared pathological. These changes are similar to histopathological changes observed following in vivo organotin administration and may represent one target of acute alkyltin ototoxicity.

Animals↗
PubMed1997

Conformational order of specific phospholipids in human erythrocytes: correlations with changes in cell shape.

Acyl chain perdeuterated dimyristoylphosphatidylcholine (DMPC-d54) and dimyristoyphosphatidylserine (DMPS-d54) were incorporated into human erythrocytes. Light microscopy demonstrated that erythrocytes incubated with an equimolar mixture of DMPC-d54/DMPS or DMPC/DMPS-d54 remained mostly discocytic whereas cells incubated with either DMPC-d54 or DMPS-d54 alone became echinocytic or stomatocytic, respectively. Cells in which the aminophospholipid translocating protein was inhibited became echinocytic when incubated with DMPS-d54. Fourier transform infrared (FTIR) spectroscopy was used to monitor conformational order in the acyl chains of the incorporated phospholipid, as detected through the asymmetric CD2 stretching vibrations in the intact cells. In cells incubated with equimolar mixtures of DMPC-d54/DMPS or DMPC/DMPS-d54, the deuterated species exhibited no thermotropic phase transitions but revealed chain order intermediate between the gel and liquid-crystal states. In contrast, DMPS-d54 incorporated into the outer leaflet of echinocytic erythrocytes was conformationally ordered while the same species incorporated into the inner leaflet of stomatocytic erythrocytes was highly disordered at all temperatures studied. Finally, DMPC-d54 incorporated into the outer leaflet of echinocytic erythrocytes exhibited a phase transition, suggesting that this species persists in domains. These data indicate that the acyl chain conformational order of specific phospholipids in the intact human erythrocyte is changed with alterations in cell morphology.

Dimyristoylphosphatidylcholine↗
PubMed1997

Transient expression of epidermal filaggrin in cultured cells causes collapse of intermediate filament networks with alteration of cell shape and nuclear integrity.

Filaggrin is an intermediate filament-associated protein (IFAP) that aggregates epidermal keratin filaments in vitro and is thought to perform a similar function during terminal differentiation in vivo. To test this function in living cells, we transiently expressed constructs encoding human filaggrin in both simple epithelial cells (COS-7) and rat keratinocytes. Scanning laser confocal microscopy showed that filaggrin-positive cells had collapsed keratin and vimentin intermediate filament (IF) networks, and that filaggrin partially co-localized with the IF networks. Filaggrin was also detected diffusely in the cytoplasm and nucleus. In contrast, when profilaggrin-like constructs, containing five filaggrin domains separated by the linker sequences, were expressed in cultured cells, immunoreactive granules formed. This finding is reminiscent of the insoluble nature of native profilaggrin that accumulates in keratohyalin granules in vivo, suggesting that the linker peptides (present in profilaggrin but not filaggrin) are important for granule formation. Cells expressing filaggrin also displayed disruption of the nucleus and the nuclear envelope; they rounded up and lost attachment to the substratum, in contrast to control cells over-expressing beta-galactosidase. This functional test of filaggrin in living cells supports its role in the reorganization and packing of keratin IF in epidermal differentiation. Moreover, the observed effects on cell morphology and nuclear integrity suggest that filaggrin may contribute to the form of apoptosis associated with terminal differentiation in epidermis.

Animals↗
PubMed2003

Fibroblast cell shape and adhesion in vitro is altered by overexpression of the 7a and 7b isoforms of protocadherin 7, but not the 7c isoform.

Protocadherins (Pcdhs) are a family of cadherins considered to play an important role in the cell-cell adhesion of specific neurons in the central nervous system. Of the reported Pcdhs, relatively little is known about the functional role of protocadherin 7 (Pcdh7), and there is no evidence of Pcdh7 mediated cell-cell adhesion. To date, three splicing variants are known; they may have different effects on cell phenotype. We report here that mouse fibroblast L cells stably overexpressing the Pcdh7 isoforms 7a and 7b, but not 7c, showed a morphological change and Ca(2+)dependent cell adhesion.

Animals↗
PubMed1999

Induction of cell shape changes through activation of the interleukin-3 common beta chain receptor by the RON receptor-type tyrosine kinase.

The RON receptor-type tyrosine kinase, a member of the hepatocyte growth factor receptor family, is a receptor for macrophage-stimulating protein (MSP). Recently, we observed that MSP induces morphological changes in interleukin (IL)-3-dependent Ba/F3 cells ectopically expressing RON. We show here that stimulation of those cells with either MSP or IL-3 increases tyrosine phosphorylation of proteins of 130, 110, 90, 62, and 58 kDa and induces similar morphological changes, accompanied by unique nuclear shape and redistribution of F-actin. A tyrosine kinase inhibitor, genistein, blocked both the increase in tyrosine phosphorylation and morphological changes. Upon stimulation with either MSP or IL-3, prominent tyrosine-phosphorylated pp90 was similarly co-immunoprecipitated with the common beta chain of IL-3 receptor (betac). Unlike IL-3, stimulation with MSP increased tyrosine phosphorylation of betac without activation of JAK2, resulting in morphological changes with modest cell growth. Confocal immunofluorescence analyses showed colocalization of RON, betac, and tyrosine-phosphorylated proteins. In vitro kinase assays revealed that autophosphorylated RON phosphorylated betac. These results suggest that the signaling pathway for morphological changes through betac and its associated protein pp90 is distinct from the pathway for cell growth in the IL-3 signal transduction system.

Actins↗
PubMed1999

The effect of quinine on outer hair cell shape, compliance and force.

Quinine intoxication causes a well-described syndrome that includes tinnitus, sensorineural hearing loss and vertigo. The pathophysiology of quinine's effects on hearing is unknown, but may include a peripheral component. The cochlear outer hair cell is known to be motile and to contribute force to amplify the vibration pattern of the organ of Corti. The outer hair cell is also a target of diseases involving tinnitus and sensorineural hearing loss, including salicylate intoxication. These effects may be mediated through changes either in motile force or in mechanical properties. Quinine's effects on outer hair cell motility and mechanical properties have therefore been examined in vitro. Quinine at 5.0 mM substantially decreased active force generation in isolated guinea pig cochlear outer hair cells. Isolated cells also elongated and dilated in diameter when exposed to 5.0 mM quinine. No consistent changes in mechanical properties were observed. 1.0 mM quinine was ineffective in either force reduction or elongation. Trifluoperazine, a calmodulin inhibitor, and ML-9, a blocker of myosin light chain kinases, were ineffective in blocking quinine-induced force reduction or elongation. Deferoxamine, a hydroxyl free radical scavenger, also failed to block either the force decrease or the elongation.

Animals↗
PubMed1994

Fission yeast protein kinase C gene homologues are required for protoplast regeneration: a functional link between cell wall formation and cell shape control.

Two novel protein kinase C (n PKC) gene homologues, pck1+ and pck2+ were isolated from the fission yeast Schizosaccharomyces pombe (Toda et al. (1993) EMBO J. 12, 1987). We examined the functional differences of pck1+ and pck2+ in cell wall formation and actin organization of S. pombe. Regenerating protoplasts of a wild-type strain, single gene disruptants of pck1+ (delta pck1) and pck2+ (delta pck2) were used as a simple model to examine the functional links between PKC, cell wall formation and actin organization. Protoplasts of the wild-type strain and those of delta pck1 reverted to intact cells in osmotically stabilized liquid medium. A close spatial association between new cell wall formation and actin was observed in these two strains. In delta pck2, protoplasts did not revert to intact cells: (1) scarcely any new cell wall material was formed; (2) actin was not reorganized; and (3) nuclear division and an increase in the amount of cytoplasm were observed in the regenerating protoplasts. These findings demonstrate that the pck2+ gene has a function essential for protoplast regeneration but the pck1+ gene does not. Involvement of n PKCs in cell wall formation and actin organization was also clarified. The effect of staurosporine (a potent inhibitor of protein kinases) on regenerating protoplasts of the three strains confirmed the assumption that the pck2 protein is an in vivo target of staurosporine in the fission yeast.

Actins↗
PubMed2000

Changes in cell shape in the ventral neuroectoderm of Drosophila melanogaster depend on the activity of the achaete-scute complex genes.

In the embryonic ventral neuroectoderm of Drosophila melanogaster the proneural genes achaete, scute, and lethal of scute are expressed in clusters of cells from which the neuroblasts delaminate in a stereotyped orthogonal array. Analyses of the ventral neuroectoderm before and during delamination of the first two populations of neuroblasts show that cells in all regions of proneural gene activity change their form prior to delamination. Furthermore, the form changes in the neuroectodermal cells of embryos lacking the achaete-scute complex, of embryos mutant for the neurogenic gene Delta, and of embryos overexpressing l'sc suggest that these genes are responsible for most of the morphological alterations observed.

Animals↗