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PubMed1990

Differential control of tropomyosin mRNA levels during myogenesis suggests the existence of an isoform competition-autoregulatory compensation control mechanism.

We have isolated tropomyosin cDNAs from human skeletal muscle and nonmuscle cDNA libraries and constructed gene-specific DNA probes for each of the four functional tropomyosin genes. These DNA probes were used to define the regulation of the corresponding mRNAs during the process of myogenesis. Tropomyosin regulation was compared with that of beta- and gamma-actin. No two striated muscle-specific tropomyosin mRNAs are coordinately accumulated during myogenesis nor in adult striated muscles. Similarly, no two nonmuscle tropomyosins are coordinately repressed during myogenesis. However, mRNAs encoding the 248 amino acid nonmuscle tropomyosins and beta- and gamma-actin are more persistent in adult skeletal muscle than those encoding the 284 amino acid nonmuscle tropomyosins. In particular, the nonmuscle tropomyosin Tm4 is expressed at similar levels in adult rat nonmuscle and striated muscle tissues. We conclude that each tropomyosin mRNA has its own unique determinants of accumulation and that the 248 amino acid nonmuscle tropomyosins may have a role in the architecture of the adult myofiber. The variable regulation of nonmuscle isoforms during myogenesis suggests that the different isoforms compete for inclusion into cellular structures and that compensating autoregulation of mRNA levels bring gene expression into alignment with the competitiveness of each individual gene product. Such an isoform competition-autoregulatory compensation mechanism would readily explain the unique regulation of each gene.

Animals↗
PubMed1992

Cell lineages, developmental timing, and spatial pattern formation in embryos of free-living soil nematodes.

From soils of various origins we have isolated a number of nematode strains and cultured them on agar plates. We have analyzed their anatomy, reproduction, and particularly their pattern of embryogenesis. With respect to early cleavage we can define six different classes. The basic scheme of embryogenesis is similar in all strains but considerable differences were observed in detail. Embryogenesis is more than five times longer in the slowest strain than in the fastest. The following general correlation was found: The slower embryogenesis proceeds in a strain, the relatively earlier the cleavage of germline cells occurs. In the fastest strain the primordial germ cell P4 is present at the 24-cell stage, while in the slowest strain it is already generated in the 5-cell stage. We hypothesize that germline cleavages have to occur within a certain time limit to preserve germline quality. The typical reversal of cleavage polarity in the division of the germline cell P2 is absent in the slowest, on other grounds apparently more primitive strain. This results in an unusual spatial arrangement of cells transiently. However, prior to gastrulation as a consequence of compensatory cell migrations (which may indicate the necessity for cell interactions), the pattern becomes very similar to that in the other strains. We propose that a standard cellular configuration is required at the beginning of gastrulation to ensure normal further development. Early cell interactions might be necessary to achieve this standard pattern. In about half of the analyzed strains cellular structures can be marked with an antibody raised against germline-specific granules of Caenorhabditis elegans. Our results do not support the notion that the staining pattern for P granules is a useful indicator for phylogenetic relationship.

Animals↗
PubMed1984

The contribution of calcium and potassium to the alpha-action of adrenaline on smooth muscle cells of the portal vein, pulmonary artery and taenia caeci of the guinea-pig.

The role of calcium and potassium in the alpha-action of adrenaline in pulmonary artery and portal vein was compared with that in taenia caeci by measuring changes in membrane potential, muscle contraction and ion fluxes in quiescent preparations from guinea-pigs (23 degrees C). The depolarization evoked by adrenaline (5 x 10(-8)-3 x 10(-5) M) was sustained in portal vein; in pulmonary artery it declined to a constant level after reaching an initial maximum. In calcium-free medium (20 min) containing EGTA (0.4 mM) and high magnesium (6.2 mM) adrenaline did not affect the membrane potential or the contractile state of the portal vein. Under these conditions the sustained phase of the response was abolished in the pulmonary artery; the remaining transient depolarization and contraction could be evoked only once. Adrenaline (3 x 10(-5) M) caused an increased 45Ca loss and 86Rb loss from the pulmonary artery and taenia caeci in calcium-free solution; a second addition of adrenaline to the calcium-free solution did not enhance the 45Ca loss from these tissues. The portal vein responded with an enhanced 86Rb loss on addition of the alpha-agonist. The bee toxin apamin (3 x 10(7) M) did not modify the depolarization, the contraction or the 45Ca and 86Rb fluxes evoked by adrenaline in the blood vessels. Enhancement of the 86Rb loss from taenia in the presence of adrenaline was prevented by apamin, but the excess loss of 45Ca was not abolished. It is concluded that adrenaline enhances cytoplasmic calcium by promoting calcium entry from the extracellular space in portal vein. In pulmonary artery and taenia caeci this is accompanied by mobilization of calcium from a cellular structure. Calcium entry facilitates triggering of the contractile proteins in vascular smooth muscle and is associated with membrane depolarization; in taenia caeci the mobilization of calcium caused by alpha-receptor activation is associated with the opening of potassium channels producing hyperpolarization and accordingly relaxation of the smooth muscle cells.

Animals↗
PubMed1987

The action of procainamide and quinidine on the alpha 1-receptor-operated channels in smooth muscle cells of guinea-pig taenia caeci.

The effect of procainamide (2.0-5.0 mM) and quinidine (0.2-1.0 mM) on the alpha 1 response evoked by adrenaline (3 X 10(-6) M) in smooth muscle cells of guinea-pig taenia caeci (22 degrees C) was studied in the presence of yohimbine (3 X 10(-6) M), propranolol (3 X 10(-6) M) or atropine (10(-6) M). The electrotonic potential elicited by the application of a constant current to the preparation was slightly increased (about 10%) by procainamide (5.0 mM) but not by quinidine (1.0 mM). The double-sucrose gap method was used for measurements. The alpha 1 response evoked by adrenaline in the absence of extracellular calcium (15 min) was represented by a transient hyperpolarization of the muscle cells, while the hyperpolarization elicited in the presence of calcium was sustained. The hyperpolarization is caused by enhancement of the potassium efflux assumed to be linked with mobilization of calcium form a cellular structure. Superfusion of the preparation with calcium-containing solution to replenish the calcium store in the presence of procainamide (10 min) before the alpha 1 response evoked in the absence of calcium and procainamide did not affect the transient hyperpolarization. Quinidine, however, suppressed the alpha 1 response when the same procedure was followed. Both the transient and the sustained hyperpolarization evoked in smooth muscle cells in the presence of procainamide (15 min) or quinidine in calcium-containing or in calcium-free solution, respectively, were inhibited. The alpha 1 response was reflected by a depolarization of the muscle cells after the potassium channels had been blocked with apamin (3 X 10(-7) M, 20 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Modulation of metabolism in HepG2 cells upon treatment with cyclosporin A and Nva2-cyclosporin.

HepG2 cells were cultured in the presence of different concentrations of cyclosporin A (CsA) or Nva2-cyclosporin (Nva2-Cs) for up to 20 days. At a low concentration (2 micrograms/ml) of CsA or Nva2-Cs, the [3H]thymidine incorporation into DNA and the rate of incorporation of [3H]leucine into total protein decreased by 20-25%. Concentrations of 10 micrograms/ml resulted in a 70% reduction of the [3H]thymidine incorporation in comparison with controls. Low concentrations of CsA resulted in mitochondria in the condensed state together with autophagosomes, large vacuoles, and elevated numbers of coated vesicles, as shown by electron microscopy. Low concentrations of Nva2-Cs resulted in swollen mitochondria, increased autophagocytosis, and increased numbers of intermediate filaments and microtubules. Higher doses of these substances (5 micrograms/ml) caused disarrangement of mitochondrial cristae, vesiculation of the endoplasmic reticulum, an elevated number of free polysomes, and accelerated autophagocytosis. Labeling of phospholipids and triglycerides with [3H]glycerol and of cholesterol and dolichol with [3H]acetate was decreased after exposure of HepG2 cells to CsA, or, in particular, Nva2-Cs. Phospholipids secreted from the cells into the medium exhibited an increased level of labeling, but the specific radioactivity of the neutral lipids in the medium was significantly decreased. Treatment of HepG2 cells with either CsA or Nva2-Cs doubled the mitochondrial cytochrome oxidase and carnitine acetyl-transferase, as well as microsomal NADPH-cytochrome c reductase activities. Such treatment also increased the cyanide-insensitive beta-oxidation of fatty acids in peroxisomes, as well as cytoplasmic DT-diaphorase and glutathione transferase activities. Prolonged treatment of the cells with CsA did not result in any cumulative effect. HepG2 cells appear to be suitable for studying the effects of cyclosporins on cellular structure and metabolism and in this system the two drugs studied here exhibited similar effects.

Carcinoma, Hepatocellular↗
PubMed1992

Lectin-induced differentiation of transformed neuroretinal cells in vitro.

The orderly course of chick neuroretinal cell differentiation was disrupted in vitro by infection with a temperature-sensitive strain of the Rous sarcoma virus (LA29). The resulting cell culture LA29NR remained mitotically active at 42 degrees C, yet rapidly adopted a transformed phenotype upon activation of the pp60v-src oncogene product at 37 degrees C. As a further indication of metabolic state, LA29NR cells expressed the protooncogene product c-Fos, as shown by Western blot analysis. Highly proliferative LA29NR cells proved refractory to standard differentiation agents such as cAMP, and prostaglandin E1. In our novel approach, succinylated concanavalin A (SCA), a nontoxic derivative of the lectin concanavalin A, induced dramatic, reversible morphological changes in LA29NR cells, including neurite outgrowth and increased cell-to-cell adhesion. Fluoresceinated SCA appeared to localize to Golgi and lysosomal structures. Cellular response to SCA treatment included decreased growth rate, reversible decrease in the phosphorylation state of a 41-kDa phosphoprotein, and induction of neuron-specific enolase. The glial marker vimentin was also evident in these cultures. These data suggest that SCA is an effective differentiation agent for cells of neuroectodermal origin, permitting neuronal as well as glial phenotypic expression within these cell populations.

Alprostadil↗
PubMed1983

Evidence for coordinated phosphorylation of keratins and vimentin during mitosis in transformed human amnion cells. Phosphate turnover of modified proteins.

Two-dimensional gel electrophoresis (IEF) analysis of short-term [32P]orthophosphate-labelled intermediate-sized filament proteins (keratins and vimentin) from transformed mitotic amnion cells (AMA), have shown that these proteins are modified coordinately and that the half life of the phosphate is about 13 min for the keratins and 11 min for vimentin. These results support the notion that the preferential modification of intermediate-sized filament proteins during mitosis may play a role in modulating filament associations with organelles and other cellular structures.

Amnion↗
PubMed1986

Lectin binding to distinguish cell types in fixed atherosclerotic arteries.

In order to assess the possible utility of lectin binding to identify the cellular components of fixed arterial lesions we studied lectin binding in experimental rabbit and monkey vessels, as well as in human atherosclerotic arteries obtained at surgery. The avidin-biotin-peroxidase technique was used to localize the binding of the following biotinylated lectins: Concanavalin A (Con A), Dolicho biflorus agglutinin (DBA), soybean agglutinin (SBA), peanut agglutinin (PNA), Phaseolus vulgaris agglutinin (PHA), Ricinus communis agglutinin (RCA), wheat germ agglutinin (WGA), and Ulex europaeus agglutinin (UEA). PHA demonstrated specific cytoplasmic staining of macrophages in rabbit, monkey, and human tissues and differentiated macrophages from other cell types in atherosclerotic lesions. When morphometric comparisons were made between lesion PHA staining and another macrophage marker, acid lipase, very similar results were obtained. Con A, RCA, and WGA stained macrophages intensely and differentiated them from other cell types in normal reticuloendothelial tissues and lesions, but also stained smooth muscle cells and endothelial cells when these cells developed lipid vacuoles. UEA stained the endothelium of vasa vasorum consistently in human arteries, but staining of artery lumen endothelium was variable. Endothelial cells of rabbit or monkey vessels did not stain with UEA. DBA, PNA, and SBA did not consistently stain any cellular structures in arteries. PHA was found to be an excellent marker to differentiate and quantify macrophages in glutaraldehyde or formalin-fixed, paraffin-embedded experimental and human atherosclerotic lesions. Con A, RCA and WGA merit further detailed study in conjunction with other histochemical tests as possible markers of functional changes in arterial cells during lesion development.

Animals↗
PubMed1989

Binding studies of the antiglucocorticoid RU38486 in Daudi and Raji lymphoma cells.

The activity of RU38486 has been studied in Burkitt's lymphoma cells which are Epstein-Barr virus (EBV) positive. The early antigens (EA) of the virus are induced by dexamethasone (DXM) in Daudi but not in Raji cells, whereas a growth factor (transforming growth factor-beta, TGF-beta) induces the EA in both cell lines. RU38486 blocks the EA induction obtained by DXM or by TGF-beta in either cell line. In order to understand the interaction of RU38486, we considered its binding to specific receptors. We first investigated the binding of the antagonist in whole cells at 22 degrees C. A number of specific binding sites higher for RU38486 than for DXM was found, suggesting that RU38486 may bind to the glucocorticoid receptor and also to other cellular structures which we called the antiglucocorticoid binding sites ("AGBS"). To support this hypothesis, competition experiments have been conducted between RU38486 and other steroid hormones (progesterone and testosterone) since it is known that RU38486 is also able to interact with their cognate receptors. Binding studies of RU38486 in vitro at 4 degrees C in the presence of cytosolic extracts from Daudi and Raji cells led to conclusions similar to those drawn from the whole cell experiments: more complexes were formed with RU38486 than with DXM. Finally, the steroid-receptor complexes were incubated with DNA-cellulose. Since the binding measured for RU38486 was higher than for DXM, we suspect that sites different from the classical glucocorticoid receptor sites are also able to interact with DNA. The blockage exerted by RU38486 on the EA induced by glucocorticoids or by non-steroidal molecules and the lack of responsiveness to glucocorticoids in Raji cells are discussed in the light of the present findings.

Binding, Competitive↗
PubMed1977

Biosynthesis of thyroid hormone: basic and clinical aspects.

Thyroid hormone formation requires the coincident presence of peroxidase, H2O2, iodide, and acceptor protein at one anatomic locus in the cell. The peroxidase enzyme appears to be a protoporphyrin lX containing heme protein, with binding sites for both iodide and tyrosine. It is probable that both iodide and tyrosine are oxidized to free radical forms which unite to form iodotyrosine. The peroxidase is also involved through an uncertain mechanism in iodotyrosine coupling and probably in oxidation of sulfhydryl bonds in thyroglobulin. H2O2 may be supplied by microsomal NADPH-cytochrome c reductase or NADH-cytochrome b5 reductase. Other possible intracellular H2OI generating systems include monoamine oxidase and xanthine oxidase. The usual acceptor for iodide is thyroglobulin, which is currently believed to be iodinated within apical secretory vesicles at the cell border just prior to liberation into the colloid, or possibly after liberation into the colloid. Other soluble an insoluble proteins are also iodinated within the gland. The peroxidase is present in numerous cellular structures, but iodination activity occurs primarily, if not only, at the apical cell border. The controls of iodination are imperfectly known. Thyrotrophin modulation of iodide uptake, H2O2 generation, thyroglobulin synthesis, and peroxidase enzyme level obviously are the main regulations. Many of these actions are thought to involve mediation of adenyl cyclase and subsequent activation of intracellular phosphokinases. Antithyroid drugs of the thiocarbamide group are competitive inhibitors of iodination under some circumstances, but if much iodide is present, they react with the oxidized iodine intermediate and are irreversibly inactivated themselves. Clinical problems involving defective peroxidase function are among the most frequent hereditary defects of thyroid hormone formation. Recognized abnormalities include deficient peroxidase, abnormality in binding of the peroxidase apoprotein to its prosthetic group, and other less well-identified abnormalities in peroxidase structure and function. Peroxidase is typically elevated in thyroid tissue from patients with hyperthyroidism sometimes deficient in cold thyroid nodules, and frequently diminished in tissue from patients with Hashimoto's thyroiditis.

Animals↗
PubMedDate not supplied

Estrogen synthetase (aromatase) in cultured human term placental cells and neoplastic human trophoblast.

Estrogen synthetase (aromatase) is present in large amounts in human term placenta. However, the localization of aromatase within the cellular structure of the placental villus is obscure. By immunocytochemical techniques using antibodies that separately recognize each component of the aromatase cytochrome P-450 enzyme system, the fraction of term placental trophoblast cells in primary culture expressing each aromatase component antigen increased from 20% in fresh mononucleated cells to about 65% for multinucleated giant cells after 72 h. In contrast, about 80% of human choriocarcinoma cells in continuous culture (JAr line) expressed each aromatase component antigen. The fraction of trophoblast cells in primary culture containing human chorionic gonadotropin increased from about 14% in fresh mononucleated cells to about 45% after 72 h and was about 30% in the choriocarcinoma cells. Fibroblast cells in culture, derived from trypsin-treated placental villi, contained aromatase activity, albeit much lower than term placental trophoblast cells. Aromatase specific activity in these placental fibroblasts did not change following growth with dibutyryl cAMP plus theophylline for 72 h.

Aromatase↗
PubMed1978

Scanning electron microscopy of the channel catfish olfactory lamellae.

The olfactory lamellae of the channel catfish (Ictalurus punctatus) are composed of sensory and indifferent (non-sensory) epithelia organized into two distinct regions on both surfaces of each lamella. The smaller sensory region located adjacent to the midline raphe has fewer cilia per unit surface area than the indifferent epithelium and contains the olfactory neurons whose ciliated dendritic terminals occur at the epithelial surface. The indifferent epithelium, comprising the greater surface area of the olfactory lamella, is covered with a dense mat of non-sensory cilia. Fractured carbon dioxide critical point dried lamellar tissue revealed the underlying cellular structure. The lamellae are composed of two layers of epithelium enclosing a thin stromal layer. Olfactory receptors were observed in the fractured tissue only within the sensory epithelium.

Animals↗
PubMed1989

Myonecrosis induced in mice by a basic myotoxin isolated from the venom of the snake Bothrops nummifer (jumping viper) from Costa Rica.

The mode of action of a basic myotoxin isolated from Bothrops nummifer venom was studied. This myotoxin is a basic polypeptide of 13,000 mol.wt, with a high content of lysine and aspartate, as well as of hydrophobic amino acids. It lacked phospholipase A2 activity when tested on several substrates at different pH values. Upon i.m. injection into mice, the toxin induced early morphological alterations typified by 'delta lesions' in the periphery of muscle fibers, an indication that the plasma membrane was the first cellular structure to be affected. Afterwards, necrotic cells had a clumped appearance, which then changed to a more hyaline histological pattern. Removal of necrotic material by phagocytes was followed by skeletal muscle regeneration, with the presence of myoblasts, myotubes and fully regenerated myofibers. The toxin induced a rapid and drastic drop in muscle creatine and creatine kinase contents of injected muscle, as well as an increase in serum levels of the enzymes lactic dehydrogenase and creatine kinase. Moreover, total muscle calcium increased significantly after toxin administration. Myotoxin induced a dose-dependent release of peroxidase entrapped in liposomes made from muscle phospholipids. The lack of phospholipase A2 activity in this toxin, together with the observation that it behaved as an amphiphilic protein in charge-shift electrophoresis, suggests that it might penetrate and disorganize muscle plasma membrane by means of a hydrophobic interaction.

Animals↗
PubMed1983

Transcriptive complex of Newcastle disease virus. I. Both L and P proteins are required to constitute an active complex.

Virions of Newcastle disease virus (NDV) were disrupted with Triton X-100 in the presence of high salt and nucleocapsids were isolated by ultracentrifugation. The nucleocapsids had very low transcriptase activity and contained only NP as a prominent protein constituent, the bulk of L and P proteins not being retained. The L and P proteins were isolated by sequential treatment of the virions with low- and high-salt detergent followed twice by successive chromatography on phosphocellulose column and examined for their effect on RNA synthesis in a standard transcriptase system using the nucleocapsids as template. When both L and P proteins were added to the template, the RNA synthetic activity was greatly stimulated. P protein alone could not enhance but rather suppressed the activity. L protein exhibited stimulation to some extent but due to residual small amount of P protein in both L protein fraction and the template it has not been elucidated whether L protein could function as a polymerase by itself. These results indicate that both L and P proteins are required to reconstitute a fully active transcriptive complex with a functional template. Attempts have been made to isolate intracellular transcriptive complex from NDV-infected MDBK cells and to determine the protein species involved. The active complex has been recovered neither from cytoplasmic extract obtained by hypotonic disruption nor from Triton X-100 soluble fraction of the cells. However, we could isolate the complex from an extract by double detergents (Tween 40 and deoxycholate) solubilization. The complex contained L, P, and NP as virus specific proteins and several cellular proteins. These results support the concept that both L and P proteins are required for NDV-RNA synthesis and suggest further that the intracellular transcriptive complex may be associated with some cellular structure resistant to Triton X-100 but sensitive to the double detergents, presumably cytoskeletal frame work.

Animals↗
PubMed1987

Psychophysical determination of intraocular light scatter as a function of wavelength.

Intraocular scatter of monochromatic light was assessed in three subjects (ages 21, 38, and 43) using the equivalent veil technique. For an annular stimulus of 3 deg inner and 8 deg outer diameter, the scattered illuminance at the center averaged 1.2% of the surround and was independent of wavelength from 420 to 650 nm. These results are inconsistent with predictions of wavelength dependence inherent in recent theories of ocular scatter. We conclude that intraocular scatter is produced by particles or cellular structures substantially larger than the wavelength of light.

Adult↗
PubMed1992

Ontogenic characteristics of cavian aldolase.

In order to extend the available information on the ontogenic significance of the interactions between aldolase and cellular structure, the nature and extent of these associations have been studied in the tissues of the guinea pig during development, along with analyses of the isozyme status in the bound and soluble compartments. In all tissues investigated, a significant degree of binding was evident, along with a considerable variation in the degree of association of aldolase with structure during development. Binding was particularly extensive in the early foetal stages and, in general, binding preference was directed towards A-type activity over the B- and C-type of enzyme. The significance of these ontogenic phenomena have been discussed in relation to the variations in phenotype of individual tissues during maturation and the metabolic correlations of this biphasic micro-organization.

Animals↗
PubMed1993

Studies on the mechanism of the cytotoxic action of the mitomycin antibiotics in hypoxic and oxygenated EMT6 cells.

The mitomycin antibiotics, because of their preferential toxicities for hypoxic cells, have significant potential as adjuncts to ionizing radiation in the treatment of solid tumors. To gain information on the mechanism by which these agents exert their cytotoxicities to hypoxic and aerobic cells, the effects of MC, POR and several of their analogs were studied in EMT6 mammary carcinoma cells. The rate of uptake of POR by these cells was directly correlated with the cytotoxicity produced by this agent under both hypoxia and aeration. At equivalent concentrations, uptake of POR into hypoxic cells was more rapid than into aerobic cells. Hypoxic cells also accumulated the antibiotic in concentrations well in excess of that present in the extracellular medium, presumably as a result of reductive activation and covalent binding of POR to cellular structures. Such activation and binding occur to a much lesser degree in aerated cells, resulting in the rapid efflux of POR from these cells when the antibiotic is removed from the extracellular environment. To gain information on the reaction of POR with DNA, mono- and bis-adducts formed in EMT6 cells exposed to this agent were measured. Three major adducts were formed. Two were mono-adducts consisting of deoxyguanosine linked at its N2-position to the C-1 of POR and of 10-decarbamoyl POR. The third was a bis-adduct in which POR was cross-linked to two deoxyguanosines at their N2-positions. More adducts were formed in hypoxia than in air, and more bis-adducts were present in hypoxic cells. Simultaneous exposure of cells to both POR and DIC reduced the total adduct level and a new unknown adduct was formed, primarily under hypoxia. Several mitomycins were evaluated for their capacity to kill EMT6 cells and to produce DNA cross-links in both hypoxia and aeration. The number of cross-links required to produce a given amount of cell kill was similar, regardless of the mitomycin employed or the degree of oxygenation. The findings support the concept that DNA is a critical target in the action of the mitomycins and that cross-linking of the DNA creates an important lesion for cytodestruction.

Animals↗