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PubMed2000

Cell membrane changes of structure and function in protein kinase inhibitor-induced polyploid cells.

Exogenous cyclic AMP has been thought to be a chemical without marked pharmacological effect until now, as it is not capable of penetrating the cell membrane in most eucaryotic cells. The present study obtained results consistent with those of most previous studies, showing that exogenous cyclic AMP itself did not interfere with the cell cycle even at the high dose of 100 microM. However, it was found that K252a, a potent inhibitor of protein kinases including protein kinase C, induced DNA re-replication, i.e. DNA synthesis at a elevated DNA ploidy in cells that had not undergone cytokinesis (leading to polyploidization), and that exogenous cyclic AMP markedly potentiated the K252a-induced polyploidization at a very low dose similar to the effective dose of membrane-permeable cyclic AMP analogue dibutyryl cyclic AMP. These findings suggested that the cell membrane changed during the formation of polyploid cells. This supposition was confirmed by scanning electron microscopy to observe structural changes and by determination of cellular attachment to investigate functional changes.

Animals↗
PubMed1991

Toad urinary bladder epithelial cells contain an analogue of cytoskeletal protein 4.1.

Epithelial cell polarity and vectorial transport require cytoskeletal proteins that maintain local cell membrane structure and mediate cytoplasmic vesicle movement. The cytoskeleton of leaky epithelia, such as the intestinal mucosa and renal proximal tubule cells, has been extensively studied. However, cytoskeletal studies in tight epithelia such as the mammalian collecting duct and toad urinary bladder generally have been confined to ultrastructural investigation. Recent research in nonepithelial cell types has identified an interesting family of cytoskeletal proteins. Present in multiple cell types, these protein 4.1 analogues share a number of similar functional characteristics, yet are structurally diverse. They are multiply phosphorylated by several different kinases, and phosphorylation regulates their associations with other cytoskeletal constituents, integral membrane components, and cytoplasmic vesicles. Using a combination of immunochemical and immunofluorescent techniques, we have demonstrated that toad bladder epithelial cells contain a 65-kDa analogue of human erythrocyte protein 4.1. Toad bladder epithelial cell protein 4.1 is structurally similar to its erythrocyte counterpart and is phosphorylated. This protein 4.1 species is present throughout the toad bladder granular cell cytoplasm, suggesting that it participates in multiple granular cell functions.

Animals↗
PubMed1982

Doxorubicin cytotoxicity enhanced by local anesthetics in a human melanoma cell line.

Local anesthetics may influence cell membrane structure and permeability. An established human melanoma cell line (SHG) derived from malignant ascites was used to evaluate the growth-inhibitory effects of local anesthetics (procaine and lidocaine) as well as of doxorubicin at incubation temperatures of 37.5 degrees C and 40 degrees C. In this system, procaine and lidocaine inhibited growth at 0.82 mg/ml and doxorubicin inhibited growth at 28 ng/ml. Noninhibitory concentrations of procaine (0.64 mg/ml) when combined with noninhibitory concentrations of doxorubicin (10 ng/ml) resulted in marked growth inhibition. Incubating temperatures of 40 degrees C enhanced all effects of procaine and doxorubicin on cell growth. These results suggest that clinically achievable concentrations of local anesthetics enhance doxorubicin cytotoxicity.

Cell Line↗
PubMed1955

The fine structure of the gall bladder epithelium of the mouse.

Sections of mouse gall bladder epithelium fixed by perfusion with buffered osmium tetroxide have been studied in the electron microscope as an example of simple columnar epithelium. The free surface presents many microvilli, each presenting a dense tip, the capitulum, and displaying a radiating corona of delicate filaments, the antennulae microvillares. Very small pit-like depressions, representing caveolae intracellulares, are encountered along the cell membrane of the microvilli. The free cell surface between microvilli shows larger cave-like depressions, likewise representing caveolae intracellulares, containing a dense material. The lateral cell borders are extensively folded into pleats, which do not interdigitate extensively with corresponding folds of the adjacent cell membrane. The terminal bars are shown to consist of thickened densities of the cell membrane itself in the region of insertion of the lateral cell wall with the free cell surface. This thickening is associated with an accumulation of dense cytoplasmic material in the immediate vicinity. The terminal bar is thus largely a cytoplasmic and cell membrane structure, rather than being primarily intercellular in nature. The basal cell membrane is relatively straight except for a conical eminence near the center of the cell, projecting slightly into the underlying tunica propria. The basal cell membrane itself is overlain by a delicate limiting membrane, which does not follow the lateral contours of the cell. Unmyelinated intercellular nerve terminals with synaptic vesicles have been encountered between the lateral walls of epithelial cells. A division of the gall bladder epithelial cell into five zones according to Ferner has been found to be convenient for this study. The following cytoplasmic components have been noted, and their distribution and appearance described: dense absorption granules, mitochondria, Golgi or agranular membranes, endoplasmic reticulum or ergastoplasm, ring figures, and irregular dense bodies, perhaps lipoid in nature. The nucleus of these cells is also described.

Animals↗
PubMed1989

An electrophysiological freeze fracture assessment of cadmium nephrotoxicity in vitro.

Human proximal tubule cell cultures exposed to doses of cadmium chloride (CdCl2) between 0.05 microgram/ml and 0.5 microgram/ml exhibited alterations in cell membrane structure and transport function. At these Cd concentrations, cell numbers were not significantly altered from control values in either nonreplicating confluent, or actively replicating subconfluent cultures. Transmission electron microscopy revealed few alterations in cultures treated with 0.05 microgram/ml Cd. Tight junctions were intact; organelles and myeloid body formation appeared normal. Freeze fracture analysis confirmed the integrity of the tight junctions as well as increased numbers of vesicles or pits along the lateral cell membrane, indicating increased endocytotic activity. Cells exposed to 0.1 microgram/ml Cd were characterized by decreased numbers of microvilli and inhibited myeloid body formation. Cd doses of 0.5 micrograms/ml elicited nuclear chromatin condensation, fragmented sealing strands in 5 to 10% of the tight junction profiles, sparse microvilli, and inhibited myeloid body formation. Electrophysiologic assessments of transport function by Ussing chamber analysis revealed decreases in transepithelial potentials for all three concentrations, with significant differences at Cd concentrations of 0.5 to 0.1 micrograms/ml. Cells treated with 0.5 micrograms/ml Cd also exhibited slight decreases in electrical resistance, consistent with the minimal fragmentation of sealing strands observed in freeze fracture replicas. Resistance in cultures treated with 0.1 or 0.05 micrograms/ml Cd remained within control values and indicated that drops in potential difference and short circuit current in these cells reflected true alterations in ion transport.

Biological Transport↗
PubMed2006

Electron tomography of ER, Golgi and related membrane systems.

A primary goal of cell biology is to uncover the mechanisms of cellular processes. A detailed structural understanding of the organelles and subcellular structures involved in these processes has often formed the foundation for the elucidation of their function. Electron tomography is a powerful technique for characterizing subcellular architecture and structural details in three dimensions. Electron tomography of cryofixed, freeze-substituted, and plastic-embedded samples allows three-dimensional visualization and display of dynamic, pleiomorphic structures at a resolution of approximately 7 nm in cell volumes up to approximately 25 microm(3). In this review, we describe the electron tomography protocols that we have employed to determine the 3D architecture of complex cellular structures, thereby gaining insights into their functional organization. We stress the need for studying specimens preserved by cryofixation methods to obtain accurate information on the geometry and size of cellular structures. We also discuss some of the challenges associated with the staining of certain types of membranes. Finally, we provide examples of how tomographic data can be analyzed, dissected, and displayed using the tools built into the IMOD software package.

Cell Membrane Structures↗
PubMed1979

Fine structure of post-mortal tissues transformations. Preliminary observations.

The Authors have studied the ultrastructure of human skin in a particular anomalous form of post-mortal transformation: the so called corification. Some structures (cell membranes, desmosomes, mitochondria, nuclear envelopes) are well preserved, while other structures (such as endoplasmic reticulum) are upset. These observations suggested that in the corification endogenous and exogenous enzymatic actions are extremely inhibited.

Cell Membrane↗
PubMed1990

Evidence that the Auberger blood group antigens are located on the Lutheran glycoproteins.

Immunoblots of red cell membranes stained with eluates of alloanti-Aua and alloanti-Aub show that these antibodies recognize 2 membrane components from Au(a+) and Au(b+) cells, respectively. These structures, of apparent molecular weight (Mr) 79,000 and 85,000, are identical in appearance and mobility on a 10% SDS polyacrylamide gel to the Lutheran glycoproteins identified by alloanti-Lub. Like the Lutheran glycoproteins, they showed a reduction in apparent Mr of about 1,500 after sialidase treatment. Red cell membrane components immunoprecipitated by a Lutheran-related monoclonal antibody, were analysed with Lutheran and Auberger antibodies by immunoblotting. The Lutheran glycoproteins were revealed by anti-Lub in precipitates from Au(a+b-) Lu(a-b+) and Au(a-b+) Lu(a-b+) cells, by anti-Aua in precipitates from Au(a+b-) Lu(a-b+) cells and by anti-Aub in precipitates from Au(a-b+) Lu(a-b+) cells. The same components were also recognized by anti-Lua in precipitates from Lu(a+b-) cells. Thus Aua and Aub antigens appear to be carried on the same red cell membrane structures as those carrying the Lutheran determinants. These results are particularly significant in the light of the very close phenotypic association between the Auberger and Lutheran blood groups which have been shown, by one family, to be controlled by genes at separate loci.

Blood Group Antigens↗
PubMed1980

[Essential fatty acids and animal development].

With the exception of some cell strains in culture, the animal cells need w6 linoleic acid and its superior polyinsaturated derivatives for their structural growth and their multiplication. Deficiency of linoleic acid leads to growth failure, organic fraility and death of the animal. Involvement of the prostaglandins is not demonstrated. w3 linolenic acid and its superior derivatives are essential for the development of the sea animals. Linolenic acid appears also essential for the mammal nervous cells at the step of cell division anterior to myelinisation. Disponibility of the essential fatty acids for the mammal fetus is principaly assumed by the mother liver of which the metabolic activity in conversion of the precursors to superior derivatives and synthesis of transport lipoproteins is increased. Involvement of the polyunsatured acids in satisfying the structural and energetic needs of the developing animal concerns predominantly--but not exclusively--the cell membranes structure and fluidity and activity of the functional proteins (enzymes, mitochondrial oxydophosphorylation).

Animals↗
PubMed1976

Membrane-bound interferon specific cell receptor system: role in the establishment and amplification of the antiviral state.

The cell membrane, in addition to other functions, plays an important role in regulating cell metabolism governed by messenger proteins (or other substances) acting from the outside. The interferon receptor system located in the cell membrane (used as a model) might consist of two components: a binding site and an activator site. As shown by experiments based on competition between interferons for the same receptor, binding is not necessarily followed by activation of the antiviral state. It is possible that polysaccharid residues present in gangliosides play an important role in binding. A critical concentration of interferon molecules in contact with the receptors is needed to induce the antiviral state, which is thus a cooperative process. The activation and probably the amplification of the response require free membrane-bound energy and the integrity of the cytoskeletal components of the cell. Modifications in cell membrane structure can change the response to interferon; on the other hand, interferon might induce changes in the cell membrane which finally result in an altered response to toxins and, in some instances, in recovery of lost contact inhibition in transformed cells.

Adenosine Triphosphatases↗
PubMed1987

Relationship between erythrocyte volume and sodium transport in the Milan hypertensive rat and age-dependent changes.

The relationship between differences in red blood cell (RBC) volume and ion transport across the erythrocyte cell membrane were investigated in the Milan Hypertensive (MHS) and Milan Normotensive (MNS) rat strains, under different experimental conditions and during ageing. The results obtained indicate that: the difference in Na+/K+ cotransport between MHS and MNS disappear when the RBC volume of the two strains becomes equal under hypotonic swelling; MHS RBCs are osmotically more fragile than those of MNS, probably because of a different membrane structure rather than a different amount of membrane surface, and the smaller volume and the lower Na+ content of MHS RBCs are maintained throughout the life span, while Na+/K+ pump activity and Na+/K+ cotransport undergo age-dependent changes, related to the development of hypertension. All these findings suggest that a primary abnormality of the cell membrane structure of MHS, probably located in the cytoskeleton, is responsible for the cell functional alterations that we previously demonstrated to be genetically associated with MHS hypertension.

Animals↗
PubMed1985

Cholesterol distribution in cells of the stria vascularis of the mammalian cochlea and some effects of ototoxic diuretics.

The distribution of cholesterol in cells of the stria vascularis of guinea pigs and gerbils has been investigated at the ultrastructural level by incubation of tissue in filipin, followed by freeze-fracture. Verification of results has been sought by using tomatin. It is shown that in the cell body region of the marginal cells, the apical and lateral membranes reacted intensely with both agents, but the membranes of the basal processes of the marginal cells did not respond significantly to either filipin or tomatin. On basal cell membranes, filipin-cholesterol complexes were present at a high density, even within the strands of the tight-junctional network of these cells and occasionally within the gap-junctional areas also. Complexes were present on intermediate cell membranes at a lower density than on other plasma membranes that showed a positive response. Tissue from animals that had received an ototoxic diuretic, either ethacrynic acid or furosemide, was characterized by the appearance of membrane regions with closely clustered filipin complexes, suggesting some change in cell membrane structure. At an early stage following diuretic administration, such clusters were particularly noticeable on the membranes of intermediate cells. As intercellular spaces enlarged in response to the effects of diuretics, vesicles released into the extracellular spaces appeared to be cholesterol-enriched. The results are discussed in relation to known features of the structure and function of cells in the normal stria vascularis and of the changes that follow from acute diuretic ototoxicity.

Animals↗
PubMed1984

The dystrophic murine skeletal muscle cell plasma membrane is structurally intact but "leaky" to creatine phosphokinase. A freeze-fracture analysis.

Skeletal muscle cells of genetically dystrophic mice (dy/dy) of the REJ-129 Bar Harbor strain exhibit reduced cytoplasmic levels of the enzyme creatine phosphokinase (CPK) when compared with normal (+/+) mice following SDS-gel electrophoresis of sarcoplasmic proteins. This observation has been thought to reflect "leakage" of CPK from dystrophic muscle cells through lesions in the sarcolemma. The present study has employed the freeze-fracture method to examine vast expanses of sarcolemma fracture face for determination of whether lesions do exist in the membrane or an alternate route is present for extravasation of CPK from dystrophic muscle cells. Most of the dystrophic cells examined in this study appeared intact and were therefore presumed viable. The intramembrane lipoprotein particles characteristic of PF-fracture face membrane were reduced in dystrophic as compared with normal murine skeletal muscle, and the plasmalemma possessed a greatly amplified population of caveolae as compared with nondiseased sarcolemma. No abnormal structural feature of these dystrophic muscle plasma membranes could be interpreted as a perforating focal "delta" lesion, such as the structures seen in thin plastic sections by other investigators. However, a second group of cells, generally few in number, that exhibited features indicative of necrosis (and loss of viability), were seen in both thin sections and platinum replicas. These moribund cells were usually embedded in dense sheaves of connective tissue along with other dystrophic cells that lacked signs of necrosis. The cytoplasm of the necrotic muscle cells was disorganized, as was the contractile machinery. The sarcolemma showed numerous perforations, through which CPK could escape into the tissue extracellular compartment. We conclude on the basis of our observations that the "focal lesions" reported by other investigators are not a structural feature of viable dystrophic muscle cell plasma membranes and are found only in necrotic or dying cells, and that the elevated serum levels of CPK associated with muscular dystrophy may result either from escape of the enzyme through lesions present in necrotic or dying cells or by extravasation along avenues provided by the hyperplastic mass of membrane caveolae present in dystrophic sarcolemma.

Animals↗
PubMed2003

Involvement of Cdc42 and Rac small G proteins in invadopodia formation of RPMI7951 cells.

BACKGROUND: Invadopodia are membrane protrusions into the extracellular matrix by aggressive tumour cells. These structures are associated with sites of matrix degradation and invasiveness of malignant tumour cells in an in vitro fibronectin degradation/invasion assay. The Rho family small G proteins, consisting of the Rho, Rac and Cdc42 subfamilies, are implicated in various cell functions, such as cell shape change, adhesion, and motility, through reorganization of the actin cytoskeleton. We studied the roles of the Rho family small G proteins in invadopodia formation. RESULTS: We first demonstrated that invadopodia of RPMI7951 human melanoma cells extended into the matrix substratum on a vertical view using a laser scanning confocal microscope system. We confirmed that invadopodia were rich in actin filaments (F-actin) and visualized clearly with F-actin staining on a vertical view as well as on a horizontal view. We then studied the roles of Rho, Rac, and Cdc42 in invasiveness of the same cell line. In the in vitro fibronectin degradation/invasion assay, a dominant active mutant of Cdc42 enhanced dot-like degradation, whereas a dominant active mutant of Rac enhanced diffuse-type degradation. Furthermore, frabin, a GDP/GTP exchange protein for Cdc42 with F-actin-binding activity, enhanced both dot-like and diffuse-type degradation. However, a dominant active mutant of Rho did not affect the fibronectin degradation. Moreover, inhibition of phosphatidylinositol-3 kinase (PI3K) disrupted the Rac and Cdc42-dependent actin structures and blocked the fibronectin degradation. CONCLUSION: These results suggest that Cdc42 and Rac play important roles in fibronectin degradation and invasiveness in a coordinate manner through the frabin-Cdc42/Rac-PI3K signalling pathway.

Actins↗
PubMed1994

A library of yeast genomic MCM1 binding sites contains genes involved in cell cycle control, cell wall and membrane structure, and metabolism.

The Saccharomyces cerevisiae MCM1 protein, which is essential for viability, participates in both transcription activation and repression as well as DNA replication. However, neither the full network of genes at which MCM1 acts nor whether MCM1 itself mediates a regulatory response is known. Thus far, sites of MCM1 action have been identified by chance during analysis of particular genes. To identify a more complete set of genes on which MCM1 acts, we isolated a library of yeast genomic sequences to which MCM1 binds and then identified known genes within this library. Fragments of genomic DNA, bound to bacterially expressed MCM1 protein, were collected on a nitrocellulose filter, cloned, and analyzed. This selected library contains a large number of genes. As expected, it is enriched for strong MCM1 binding sites and contains cell-type-specific genes known to require MCM1. In addition, it also includes sequences upstream (or near the 5' end) of a number of identified yeast genes that have not yet been shown to be controlled by MCM1. These include genes whose products are involved in (i) the control of cell cycle progression (CLN3, CLB2, and FAR1), (ii) synthesis and maintenance of cell wall or cell membrane structures (PMA1, PIS1, DIT1,2, and GFA1), (iii) cellular metabolism (PCK1, MET2, and CCP1), and (iv) production of a secreted glycoprotein which is heat shock inducible (HSP150). The previously unidentified MCM1 binding site in the essential PMA1 gene is required for expression of a PMA1:lacZ fusion gene, providing evidence that one site is functionally important. We speculate that MCM1 coordinates decisions about cell cycle progression with changes in cell wall integrity and metabolic activity. The presence in the library of three genes involved in cell cycle progression reinforces the idea that one of the functions of MCM1 is indeed analogous to that of the mammalian serum response factor.

Base Sequence↗
PubMed1984

Comparison of the inhibitory activity of seven anti-T8 antibodies on specific cellular cytotoxicity.

To evaluate the functional significance of the T-cell membrane structure recognized by OKT8 or Leu2a, seven different monoclonal antibodies, reacting with different epitopes of this 76 KD big membrane structure, were evaluated for their ability to alter specific cell mediated lympholysis after a mixed leukocyte reaction. The stimulated effector cells were first incubated with a monoclonal antibody, washed and then tested for their cytotoxicity. Those antibodies, which react with a highly trypsin-sensitive region of the T8 glycoprotein, were the most effective inhibitors of the cytotoxicity (T811, FK18). Those antibodies, which react with a relative trypsin-resistant region (OKT8, Leu2a, WT82, WT85) or with a trypsin-sensitive epitope (WT81), which is in a close neighborhood to WT82 or WT85, appear to be able to block the cytotoxicity only in certain effector/target cell combinations. The data suggest that different regions of the T8 glycoprotein are involved in the specific cytotoxic reactions, and that the involvement of certain epitopes may depend on the effector/target cell combination.

Antibodies, Monoclonal↗
PubMed2006

Estrogen receptor alpha interacts with Galpha13 to drive actin remodeling and endothelial cell migration via the RhoA/Rho kinase/moesin pathway.

Sex steroids control cell movement and tissue organization; however, little is known of the involved mechanisms. This report describes the ongoing dynamic regulation by estrogen of the actin cytoskeleton and cell movement in human vascular endothelial cells that depends on rapid activation of the actin-regulatory protein moesin. Moesin activation is triggered by the interaction of the C-terminal portion of cell membrane estrogen receptor alpha with the G protein Galpha(13), leading to activation of the small GTPase RhoA and of the downstream effector Rho-associated kinase. The resulting phosphorylation of moesin on Thr(558) is the means of moesin's binding to actin and the remodeling of the actin cytoskeleton. This cascade of events ensues within minutes of estradiol administration and results in changes in cell morphology and to the development of specialized cell membrane structures such as ruffles and pseudopodia that are necessary for cell movement. These findings expand our knowledge of the basis of estrogen's effects on human cells, including the regulation of actin assembly, cell movement and migration. They highlight novel pathways of signal transduction of estrogen receptor alpha through nontranscriptional mechanisms. Furthermore, exposure of this estrogen receptor-dependent, nongenomic action of estrogen on human vascular endothelial cells is especially relevant to the present interest in the role of estrogen in cardiovascular protection.

Actins↗