Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cell Shape”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1988

Changes in cell shapes and cytokeratins of epithelial cells during the infiltration of lymphocytes in the human palatine tonsils.

By the immunohistochemical method using anti-keratin antibodies (KL1-antigen, 56 KD keratin; PKK1-antigen, 40-52.5 KD keratin) and electron microscopy, the changes in cell shapes and the cytokeratin components of the epithelial cells during the infiltration of lymphocytes were studied. In the surface epithelium, PKK1 reacts with only the keratinocytes in the basal layer, while KL1 stains in the spinous layer. In the neck portion of the crypt, transformed keratinocytes scattered in the spinous layer react intensely with PKK1. These cells issue prolonged cytoplasmic processes which surround the cavities filled with infiltrating lymphocytes. In the deep portion of the crypt, PKK1-positive cells interconnect with one another constituting the network of the star-shaped reticular cells. The enlarged intercellular spaces of the reticular cells are filled with many lymphocytes. Our observations suggest that the infiltration of lymphocytes into the crypt epithelium induces the change in keratin expression of the epithelial cells in the human palatine tonsils, and the change of keratin molecules makes the stratified flattened epithelium to transform into the network of star-shaped reticular cells.

Child↗
PubMed1986

Fourier analysis of the cell shape of paired human urothelial cell lines of the same origin but of different grades of transformation.

The rationale of the present investigation is the observations made by many authors of changes in the molecular structure of the cell surface during the multistep process of malignant transformation. These changes may influence cell-matrix and cell-cell interactions and thereby cause changes in cell adhesiveness and cell shape. The aim of the present work was to investigate whether the development of various grades of transformation in vivo and in vitro of human urothelial cells is accompanied by significant changes in cell shape as measured by Fourier analysis. The following transformation grades (TGr) have been defined (Christensen et al. 1984; Kieler 1984): TGr I = nonmalignant, mortal cell lines that grow independently of fibroblasts and have a prolonged life span. TGr II = nonmalignant cell lines with an infinite life span. TGr III = malignant and immortal cell lines that grow invasively in co-cultures with embryonic chick heart fragments and possess tumorigenic properties after s.c. injection into nude mice. Comparisons of 4 pairs of cell lines were performed; each pair was of the same origin. Two pairs--each including a TGr I cell line (Hu 961b and Hu 1703S) compared to a TGr III cell line (Hu 961a or Hu 1703He)--were derived from two transitional cell carcinomas (TCC) containing a heterogeneous cell population. Two additional cell lines classified as TGr II (HCV-29 and Hu 609) were compared to two TGr III sublines (HCV-29T and Hu 609T, respectively) which arose by "spontaneous" transformation during propagation in vitro of the respective maternal TGr II-cell lines.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcinoma, Transitional Cell↗
PubMed2004

Cell shape, cytoskeletal tension, and RhoA regulate stem cell lineage commitment.

Commitment of stem cells to different lineages is regulated by many cues in the local tissue microenvironment. Here we demonstrate that cell shape regulates commitment of human mesenchymal stem cells (hMSCs) to adipocyte or osteoblast fate. hMSCs allowed to adhere, flatten, and spread underwent osteogenesis, while unspread, round cells became adipocytes. Cell shape regulated the switch in lineage commitment by modulating endogenous RhoA activity. Expressing dominant-negative RhoA committed hMSCs to become adipocytes, while constitutively active RhoA caused osteogenesis. However, the RhoA-mediated adipogenesis or osteogenesis was conditional on a round or spread shape, respectively, while constitutive activation of the RhoA effector, ROCK, induced osteogenesis independent of cell shape. This RhoA-ROCK commitment signal required actin-myosin-generated tension. These studies demonstrate that mechanical cues experienced in developmental and adult contexts, embodied by cell shape, cytoskeletal tension, and RhoA signaling, are integral to the commitment of stem cell fate.

Actin Cytoskeleton↗
PubMed1988

Glutaraldehyde induces cell shape changes in isolated outer hair cells from the inner ear.

Individual isolated outer hair cells (OHCs) from the cochlea were maintained in a collagen gel and viewed in the light microscope. They were observed during fixation and processing for transmission electron microscopy and individual cells were selected for observation in the electron microscope. Application of glutaraldehyde at several concentrations caused OHCs to become shorter. Shrinkage occurred during dehydration but there was no further change during infiltration with the epoxy resin. Ultrastructural analysis of isolated cells fixed with glutaraldehyde and postfixed with osmium tetroxide showed that these cells were similar to cells fixed in the intact cochlea. The glutaraldehyde-induced cell shape change is similar to the shortening seen in intact OHCs in response to the application of solutions containing high potassium or caffeine. Application of glutaraldehyde to cells pretreated with potassium or caffeine caused further shortening. Glutaraldehyde-induced cell shape change was not blocked by the application of tetracaine, which did prevent potassium-induced and caffeine-induced shortening. Glutaraldehyde-induced cell shape change was not stopped by short treatment with N-ethylmaleimide, which did inhibit potassium-induced shortening. Results from these experiments suggest that the glutaraldehyde-induced OHC shape change is not caused by an effect on the membrane or by calcium activation of a contractile response. Shortening may be caused by shrinkage due to cross-linking of proteins.

Aldehydes↗
PubMed2000

Spindle-shaped cells derived from giant-cell tumor of bone support differentiation of blood monocytes to osteoclast-like cells.

Spindle-shaped cells were established from four giant-cell tumors of bone. When human blood monocytes were co-cultured with these cells, multinucleated giant-cell formation of monocytes was induced. Intriguingly, even when a filter (pore size: 0.45 microm) was interposed between monocytes and the spindle-shaped cells, polykaryocytes also appeared. These multinucleated giant cells were positive for tartrate-resistant acid phosphatase, expressed calcitonin receptor, and showed bone-resorption activity, characteristics of osteoclast-like cells. These findings indicate that soluble factors secreted from these cells play an important role in osteoclast-like cell formation from blood monocytes. These data additionally suggest that these cells support osteoclast-like cell formation in giant-cell tumors of bone. The cells also expressed mannose receptor, fibronectin, receptor activator of nuclear factorkappaB, and several cytokine mRNAs, including interleukin-6, receptor activator of nuclear factorkappaB ligand/osteoclast differentiation factor/osteoprotegerin ligand, and macrophage colony-stimulating factor. However, all of these molecules except receptor activator of nuclear factorkappaB ligand mRNA could also be detected in control HeLa and CV-1 cells. Although the soluble receptor activator of nuclear factorkappaB ligand has not been found under physiological conditions, it is possible that it is cleaved by cellular proteases and the truncated receptor activator of nuclear factorkappaB is released from cells. Identification of the soluble factors capable of inducing osteoclast formation from blood monocytes is a pressing problem to be solved.

Bone Neoplasms↗
PubMed1994

Regulation of alveolar epithelial cell ICAM-1 expression by cell shape and cell-cell interactions.

In normal lung, intercellular adhesion molecule 1 (ICAM-1) is expressed at high levels on thin type I alveolar epithelial cells, but is minimally expressed on cuboidal type II cells. ICAM-1 is induced in primary culture on tissue culture-treated plastic as type II cells undergo transition toward a type I cell-like phenotype. We hypothesized that alveolar epithelial cell expression of ICAM-1 might be regulated in part by signals that influence the state of differentiation of these cells. We found that rat type II cells that were cultured as aggregates of cuboidal cells on a hydrated basement membrane gel (Matrigel) or on floating type I collagen gels, expressed markedly less ICAM-1 protein and mRNA compared with cells that had spread on plastic. In contrast, type II cells that had spread as monolayers on dishes coated with basement membrane proteins in planar configuration demonstrated ICAM-1 expression comparable to that of cells on plastic alone. Thus regulation of alveolar epithelial cell expression of this immunologically important adhesion molecule involves complex spatial interactions of the cells with the basement membrane and other epithelial cells.

Animals↗
PubMed2006

UV-embossed microchannel in biocompatible polymeric film: application to control of cell shape and orientation of muscle cells.

This article shows that ultra violet (UV) micro-embossing can be successfully used for fabricating biocompatible micropatterned films with microchannels separated by high aspect ratio microwalls. Eight series of micropatterns were investigated; the width of the microwall was either 10 or 25 microm and that of the microchannel either 40, 80, 120, or 160 microm. The material investigated was principally polyurethane diacrylate. The UV-embossed micropattern was extracted with methanol, converting the micropatterns from cytotoxic to biocompatible. The typical UV embossing method was modified by using a marginally adhesive polyester substrate, which facilitates demolding but is removable before methanol extraction to avoid fragmentation of the embossed micropatterns. The effect of the micropatterns on A7r5 smooth muscle cells and C2C12 skeletal muscle cells was investigated. The dimensions of both channel and wall have significant effects on the elongation of both muscle cells. In the narrower 40-microm channel, the C2C12 cells merged together to form myofibers. These results indicate that UV-embossed micropatterns may present a useful scaffold for in vitro cell shape and orientation control needed in vascular and muscle tissue engineering.

Animals↗
PubMed1999

NO alters cell shape and motility in aortic smooth muscle cells via protein tyrosine phosphatase 1B activation.

Cell motility is an important determinant of vascular disease. We examined mechanisms underlying the effect of nitric oxide (NO) on motility in cultured primary aortic smooth muscle cells from newborn rats. The NO donor S-nitroso-N-acetyl-penicillamine (SNAP) increased the activity of protein tyrosine phosphatase 1B (PTP-1B). This effect was mimicked by a cGMP analog and blocked by the guanyl cyclase antagonist 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, indicating the involvement of cGMP. Treatment of cells with antisense, but not control oligodeoxynucleotide (ODN), against PTP-1B attenuated the inhibitory effect of NO on cell motility. Cell shape and adhesion are important determinants of cell motility. We report that SNAP induced cell rounding and reduced adhesion and caused dissociation of actin stress fibers. Moreover, SNAP reduced phosphotyrosine levels in focal adhesion proteins, paxillin, and focal adhesion kinase. The PTP inhibitor phenylarsine oxide or decrease of PTP-1B protein levels via the use of antisense ODN prevented NO-induced cell-shape change, altered adhesion, and migration. These results indicate that NO regulates cell shape, adhesion, and migration by dephosphorylation of focal adhesion proteins via a mechanism that requires PTP-1B activity.

Animals↗
PubMed1987

Effect of cell shape on proteinase secretion by epithelial cells.

Cell proliferation has been found to correlate with increased secretion of proteinases, such as plasminogen activator, in several different cell populations. In addition, the shape of the cell may also play a role in regulating proteinase secretion. However, the relationship between cell proliferation, cell shape and proteinase secretion has not been studied in diploid epithelial (E) cells cultured from porcine periodontal ligament (PL). We have modified PLE cell shape by physical means, such as growth on less-adhesive substrata and mechanical stretching, and by exposure to cholera toxin and 12-O-tetradecanoylphorbol-13-acetate (TPA). Neutral proteinase and plasminogen activator secretion were found to correlate with cell shape, the more round the cells, the greater the amount of proteinase secreted. PLE cells, stimulated to proliferate by cholera toxin or dibutyryl cyclic AMP, were more spread than control cells, but secreted less neutral proteinase and plasminogen activator. TPA stimulated cell proliferation slightly but, in contrast to cholera toxin, increased cell rounding and the secretion of neutral proteinase and plasminogen activator. Thus proteinase secretion was related more to cell shape than to cell proliferation.

Animals↗
PubMed1991

Cell-shape regulation and matrix protein p52 content in phenotypic variants of ras-transformed rat kidney fibroblasts. Functional analysis and biochemical comparison of p52 with proteins implicated in cell-shape determination.

The 52 kDa transformation-sensitive protein p52 was previously identified as a major substrate-associated component of normal rat kidney (NRK) fibroblasts [Higgins & Ryan (1989) Biochem. J. 257, 173-182]. p52 selectively localized to cellular fractions enriched in substrate focal-contact sites and associated ventral undersurface elements. Rapid attachment/spreading of NRK cells on to prepared p52 matrices and inhibition of fibroblast spreading by antibodies to p52 indicated that this protein participates in shape determination or cell-to-substrate adhesion. NRK cells transformed with Kirsten murine sarcoma virus (KiMSV), with a temperature-sensitive mutant (ts-371 KiMSV) and maintained at the permissive temperature, or with the cloned EJrasval.12 oncogene, exhibited down-regulated accumulation of p52 in the ventral undersurface region. Immunochemical, lectin-affinity and electrophoretic analyses indicated that p52 shares considerable sequence similarity with plasminogen-activator inhibitor type-1, which is consistent with its subcellular localization and likely morphoregulatory activity. The marked down-regulation of p52 expression seen in four different ras-mediated transformation systems, its induction prior to butyrate-induced morphological reorganization in KiMSV-transformed cells, and the morphological consequences of exogenously added p52 or p52 antibodies on NRK fibroblasts suggest that this protein probably functions in cell-shape regulation. Abrogation of p52 matrix accumulation typically seen in ras transformants may contribute, therefore, to the aberrant cytoarchitecture characteristic of malignant fibroblasts.

Animals↗
PubMed1987

Colchicine reverts cell shape but not collagen phenotypes in corneal endothelial cells modulated by polymorphonuclear leukocytes.

The authors have shown previously that polymorphonuclear leukocytes (PMN) modulate rabbit corneal endothelial cells (CEC) into cells that irreversibly acquire the characteristics of fibroblasts, including multilayering of spindle-shaped cells and deposition of interstitial extracellular matrix composed predominantly of type I collagen. In an attempt to determine if the changes in cell shape caused by the disruption of cytoskeleton are correlated with the alteration of collagen phenotypes in fibroblastic corneal endothelial cells (FCEC), colchicine and cytochalasin B (CB) were used. A series of dose-response studies were performed, and correlated with exposure time. When cells were exposed to the drugs (ranging from 0.01-4.0 micrograms/ml) 24 hr after plating, the majority of cells treated with colchicine dramatically changed from fibroblastic to polygonal shape: cells became flattened and cytoplasmic processes disappeared. Conversely, no apparent changes were observed in the CB-treated cells. On removal of colchicine, the cells resumed fibroblastic morphology within 24 hr; most of the cells again developed cytoplasmic processes. When collagen phenotypes were analyzed by electrophoresis, types I, III, and V collagen were present in either the colchicine or CB-treated cells, regardless of the concentration of drug used. However, synthesis of type I trimer and type III collagen was significantly increased in the cells treated with colchicine at concentrations greater than or equal to 1.0 microgram/ml; the alpha 1:alpha 2 ratio was approximately 4.5, and type III accounted for 35-40% of the total collagen. CB did not induce a similar alteration. These observations indicate that changes in cell shape are not related to the switch of collagen phenotypes in FCEC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Thrombospondin gene expression by endothelial cells in culture is modulated by cell proliferation, cell shape and the substratum.

Endothelial cells plated on the surface of a two-dimensional substratum (gelatin-coated dishes, dishes coated with native type I collagen or collagen gels) form a cobblestone monolayer at confluence, whereas cells plated within a three-dimensional gel matrix elongate into a sprouting morphology and self-associate into tube-like structures. In this study, we have compared the synthesis of thrombospondin by quiescent endothelial cells displaying (a) the same morphological phenotype (cobblestone) on different substrata (gelatin and collagen) and (b) different morphological phenotypes (cobblestone and sprouting) on the same substratum (collagen). We demonstrate that thrombospondin is a major biosynthetic product of confluent, quiescent cells cultured on dishes coated with either gelatin or collagen, and that the synthesis of this protein is markedly decreased when cells are plated on or in three-dimensional collagen gels. Moreover, we demonstrate that cells plated in gel (sprouting) secrete less thrombospondin than do cells plated on the gel surface (cobblestone). The regulation of thrombospondin synthesis is reversible and occurs at the level of transcription, as steady-state mRNA levels for thrombospondin decrease in a manner comparable with the levels of protein secreted by these cells. We also show that mRNA levels for laminin B2 chains are increased when cells are cultured on and in collagen gels compared with on gelatin-coated dishes, suggesting that the syntheses of thrombospondin and laminin are regulated by different mechanisms. When cells are cultured on gelatin- or collagen-coated dishes, thrombospondin gene expression is directly proportional to the proliferative state of the cultures. By contrast, the synthesis of thrombospondin by cells cultured on collagen gels remains at equally low levels whether they are labelled when they are sparse and rapidly proliferating or when they are confluent and quiescent. Fibronectin synthesis was found to increase with increasing confluency of the cells plated on all three substrata. These results demonstrate that thrombospondin gene expression is modulated by cell shape, cell proliferation and the nature of the substratum used for cell culture.

Animals↗
PubMed1987

Steroidogenesis in adrenal tumor cells: influence of cell shape.

Y-1 adrenal tumor cells were grown on plastic, or plastic treated with poly(2-hydroxyethyl methacrylate) (polyHEMA) to produce concentration-dependent rounding (10(-5)-3 X 10(-4) M) of the cells or on plastic treated with poly-D-lysine (polylysine) to produce flat cells, in order to determine whether or not cell shape is correlated with steroid synthesis. The degree of rounding of cells was measured by determining mean cell height and longest cell diameter. Three measurements of steroid production were made: production of 20 alpha-dihydroprogesterone, transport of cholesterol to the inner mitochondrial membrane, and production of pregnenolone by isolated mitochondria. Cells grown on poly(HEMA) showed increase in mean cell height, decrease in longest diameter (i.e. rounding), and increase in all three measurements of steroidogenesis. In the case of synthesis of 20 alpha-dihydroprogesterone, the response was dependent on the concentration of poly(HEMA), being greater with higher concentrations (up to 10(-4) M), of this agent. Moreover the degree of rounding (cell height) was correlated with production of 20 alpha-dihydroprogesterone at three concentrations of poly(HEMA) (r = 0.93. ACTH at a supramaximal concentration produced increases in all of these responses to the poly(HEMA) surface. Polylysine produced flatter cells (lower mean height and greater longest diameter) than plastic and also inhibited all three steroidogenic responses to ACTH. (Bu)2cAMP exerted the same effects as ACTH. Growing cells on poly(HEMA) or polylysine did not affect production of cyclic AMP by the cells. Addition of poly(HEMA) or polylysine to the medium in which the cells were incubated, at the same concentrations as those used for influencing cell shape, was without effect on steroid synthesis or the response to ACTH. Cells grown on poly(HEMA) show decreased incorporation of [3H] thymidine into DNA. It is concluded that cell shape influences the delivery of cholesterol to inner mitochondrial membrane and in this way, increases the production of steroids by Y-1 cells and that the effects of poly(HEMA) on cell shape, cholesterol transport, and synthesis of DNA may involve microfilaments.

20-alpha-Dihydroprogesterone↗
PubMed1986

Ionophore-induced cell shape changes in Xenopus early embryos.

Local application of the Ca++ ionophore A23187 to the intact lateral ectoderm of Xenopus early neurulae causes changes in the shapes of the cells; ectoderm cells lose their relatively flat surfaces and become rounded. Some of the affected cells form microvilli. Ionophore was found to induce cell shape changes in ectoderm in the presence of cytochalasin-B, suggesting that microfilaments are not involved. Ionophore was also found to induce cell shape changes in neurula ectoderm when it was applied to embryos cultured in Ca++- and Mg++-free medium containing EDTA, suggesting that extracellular Ca++ is not utilized in the ionophore-induced cell shape changes. Similarly, the Ca++ antagonists D-600, which reduces the entry of Ca++ into cells, and TMB-8, which antagonises certain intracellular Ca++-dependent functions, did not inhibit the effects of A23187 on amphibian embryos.

Animals↗
PubMed1998

Genetics of plant cell shape.

Plant cells have a variety of shapes crucial for their functions, yet the mechanisms that generate these shapes are poorly understood. Genetic dissection of the trichome (plant hair) branching pathway in Arabidopsis, has uncovered mechanisms and identified genes that control plant cell morphogenesis. The recent identification of one of these genes, ZWICHEL (ZWI), as a novel member of the kinesin superfamily of microtubule motors provides a starting point for the analysis of the plant cytoskeleton's role in a specific morphogenetic event.

Arabidopsis↗
PubMed1991

Animal cell shape changes and gene expression.

Cell shape and cell contacts are determined by transmembrane receptor-mediated associations of the cytoskeleton with specific extracellular matrix proteins and with ligands on the surface of adjacent cells. The cytoplasmic domains of these microfilament-membrane associations at the adherens junction sites, also localize a variety of regulatory molecules involved in signal transduction and gene regulation. The stimulation of cells with soluble polypeptide factors leads to rapid changes in cell shape and microfilament component organization. In addition, this stimulation also activates the phosphoinositide signaling pathway. Recently, a linkage between actin-binding proteins and the phosphoinositide signaling pathway, was discovered. It is suggested that by the association with the second messenger system, and/or by controlling the localization of regulatory molecules, the cytoskeleton may regulate gene expression.

Actin Cytoskeleton↗