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At least 847 records · Page 47Linked to original sources
PubMed1983

Relationship between sarcoplasmic reticulum volume and calcium capacity in skinned frog skeletal muscle fibres.

Semitendinosus fibres from Rana pipiens were examined in the electron microscope. When the aqueous solutions in which the fibres were prepared contained no sucrose, the sarcoplasmic reticulum was markedly swollen and possibly fragmented. When as little as 50 mM sucrose was included in the aqueous solution, the sarcoplasmic reticulum retained the flattened appearance characteristic of intact fibres. The degree of flattening was not substantially different with concentrations of sucrose ranging from 50 to 300 mM, suggesting that the flattened volume may be determined by structural elements. In all the fibre segments, the regularity of the hexagonal filament lattice was disrupted and the disruption was not affected by sucrose. Radioactive calcium uptake was measured in the presence and absence of 200 mM sucrose. The capacity of the sarcoplasmic reticulum (SR) was depressed by about 30% by the sucrose but the initial uptake was not significantly affected. This finding suggests that most of the calcium within the SR is bound and not free in solution.

Animals↗
PubMed1977

Effect of ethionine on the rough endoplasmic reticulum from male and female rat liver.

Ethionine causes a decrease in the amount of rough endoplasmic reticulum in rat liver, the effect being greater in female than in male rats. Rough endoplasmic reticulum isolated from rat liver 24 hr after ethionine injection and stripped of its ribosomes partially lost its in vitro ribosome binding capacity. However, no differences were detected between the binding affinities of ribosomes, isolated from either untreated animals or intoxicated rats, to stripped rough membranes derived from normal rats. Structural changes occur in the rough endoplasmic reticulum of the ethionine treated rats, while the ribosomes are still bound to the membrane.

Animals↗
PubMed1993

Tridimensional organization of Purkinje neuron cisternal stacks, a specialized endoplasmic reticulum subcompartment rich in inositol 1,4,5-trisphosphate receptors.

Stacks of regularly spaced, flat, smooth-surfaced endoplasmic reticulum cisternae frequently observed in both the cell body and dendrites of cerebellar Purkinje neurons, were previously shown by immunocytochemistry to be highly enriched in receptors for the second messenger, inositol 1,4,5-trisphosphate. Morphometric analyses have been carried out on randomly selected thin section images of rat Purkinje neurons to reveal the tridimensional organization of these structures. Individual stacked cisternae (on the average approximately 3.5 per stack) were shown to be separated from each other by a 23.5 nm space occupied by perpendicular bridges, approximately 20 nm in diameter, most probably composed by two apposed receptor homotetramer molecules, inserted into the parallel membranes in their hydrophobic domains. In the stacked membranes the density of the bridges was approximately 500 microns -2, corresponding to approximately 15% of the surface area. The lateral distribution of bridges was not random, but revealed regular distances that might correspond to unoccupied receptor slots. In each stack, the external cisternae were often in direct lumenal continuity with conventional elements of the endoplasmic reticulum, whereas the internal cisternae were not. Since continuities between stacked cisternae were never observed, the results indicate that the internal cisternae are at least transitorily discrete, i.e. they are not in permanent lumenal continuity with the rest of the endoplasmic reticulum. To our knowledge this is the first demonstration of a physical subcompartmentalization of the latter endomembrane system in a non-mitotic cells. A model for the biogenesis of cisternal stacks, based on the head-to-head binding and lateral interaction of the inositol 1,4,5-trisphosphate receptor molecules in the plane of the interacting membranes, is proposed and critically discussed.

Animals↗
PubMed1992

Giant sarcoplasmic reticulum vesicles: a study of membrane morphogenesis.

Rabbit sarcoplasmic reticulum vesicles were fused into giant proteoliposomes in a medium of 0.1 M KCl, 10 mM Tris-maleate, pH 7.0, 10 micrograms ml-1 antipain, 10 micrograms ml-1 leupeptin, 25 IU per ml Trasylol, 3 mM NaN3, 3.75% PEG 1500 and 3% DMSO by brief exposure to 37 degrees C, followed by incubation for 4 h at 25 degrees C. Approximately 5-10% of the sarcoplasmic reticulum elements underwent fusion, forming single-walled spherical vesicles of 1-25 microns diameter, in which the polarity of the native membrane was preserved. The Ca(2+)-stimulated ATPase activity remained essentially unchanged after fusion. On exposure to decavanadate in a Ca(2+)-free medium the spherical vesicles assumed a corrugated appearance with the formation of long ridges separated by deep furrows that eventually pinched off longitudinally and separated into numerous long crystalline tubules of uniform (approximately 0.1 microns) diameter. The vanadate-induced transformation of giant vesicles into tubules implies that the geometry of the sarcoplasmic reticulum membrane is determined by the conformation of the Ca(2+)-ATPase.

Animals↗
PubMed1982

Mechanism of calcium release from skeletal sarcoplasmic reticulum.

Ca2+ -induced Ca2+ release at the terminal cisternae of skeletal sarcoplasmic reticulum was demonstrated using heavy sarcoplasmic reticulum vesicles. Ca2+ release was observed at 10 mum Ca2+ in the presence of 1.25 mm free Mg2+ and was sensitive to low concentrations of ruthenium red and was partially inhibited by valinomycin. These results suggest that the Ca2+ -induced Ca2+ release is electrogenic and that an inside negative membrane potential created by the Ca2+ flux opens a second channel that releases Ca2+. Results in support of this formulation were obtained by applying a Cl- gradient or K+ gradient to sarcoplasmic reticulum vesicles to initiate Ca2+ release. Based on experiments the following hypothesis for the excitation-contraction coupling of skeletal muscle was formulated. On excitation, small amounts of Ca2+ enter from the transverse tubule and interact with a Ca2+ enter from the transverse tubule and interact with a Ca2+ receptor at the terminal cisternae and cause Ca2+ release (Ca2+ -induced Ca2+ release). This Ca2+ flux generates an inside negative membrane potential which opens voltage-gated Ca2+ channels (membrane potential-dependent Ca2+ release) in amounts sufficient for contraction.

Adenosine Triphosphate↗
PubMed1988

Correlation between the synergistic effect of liposomes and endotoxins on the activation of macrophage tumoricidal activity and the effect of liposomes on the rough endoplasmic reticulum of macrophages.

Treatment of resident peritoneal macrophages of rats with small unilamellar vesicles of dipalmitoylphosphatidylcholine (DPPC SUV) potentiated their activation for tumor cell lysis by endotoxins. The fluorescence polarization of diphenylhexatriene (DPH) embedded in rough endoplasmic reticulum membranes isolated from DPPC SUV-treated macrophages was enhanced. The average fluorescence lifetime of DPH and the rotational correlation time deduced from anisotropy decay were unchanged, whereas the residual anisotropy and hence the order parameter were increased. The measurement of the fluorescence anisotropy of DPH as a function of the temperature showed a phase transition. No phase transition was observed in the rough endoplasmic reticulum membranes of macrophages either treated or not treated with cholesterol/DPPC SUV (1/1; mol/mol). The synergistic effect of DPPC SUV on the tumoricidal activity of macrophages induced by endotoxins appears to be correlated with the changes in the properties of the rough endoplasmic reticulum membranes. Both effects were transient; they had the same kinetics of induction and reversion, and they were both inhibited by cholesterol.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1988

Activation of Ca2+ release in isolated sarcoplasmic reticulum.

The relationship between Ca2+ release from sarcoplasmic reticulum, induced by elevated pH, tetraphenylboron (TPB-) or chemical modification, and the change in the surface charge of the membranes as measured by the fluorescence intensity of anilinonaphthalene sulfonate (ANS) is examined. The simulated Ca2+ release is inhibited by dicyclohexylcarbodiimide and external Ca2+. TPB-, but not tetraphenylarsonium (TPA+), causes a decrease in ANS- fluorescence, with 50% decrease occurring at about 5 microM TPB-. The decrease in ANS- fluorescence as well as the inhibition of Ca2+ accumulation induced by TPB- are prevented by TPA+. A linear relationship between the decrease in membrane surface potential and the extent of the Ca2+ released by TPB- is obtained. Similar levels of [3H]TPB-bound to sarcoplasmic reticulum membranes were obtained regardless of whether or not the vesicles have taken up Ca2+. The inhibition of Ca2+ accumulation and the [3H]TPB- incorporation into the membranes were correlated. Ca2+ release from sarcoplasmic reticulum, by pH elevation, chemical modification or by addition of NaSCN (0.2 to 0.5 M) or the Ca2+ ionophore ionomycin, is also accompanied by a decrease in ANS- fluorescence intensity. However, chemical modification and elevated pH affects the surface potential much less than SCN- or TPB- do. These results suggest that the enhancement of Ca2+ release by these treatments is not due to a general effect on the membrane surface potential, but rather through the modification of a specific protein. They also suggest that membrane surface charges might play an important role in the control mechanism of Ca2+ release.

Anilino Naphthalenesulfonates↗
PubMed1978

Ionic permeability of sarcoplasmic reticulum vesicles measured by light scattering method.

The volume change of sarcoplasmic retriculum vesicles was followed by measuring the light scattering intensity. When the salt concentration of the suspension of sarcoplasmic reticulum vesicles was increased by using a stopped flow apparatus, the light scattering intensity rapidly increased at the beginning and then decreased. The fast increase in the light scattering intensity is caused by the decrease of the volume of sarcoplasmic reticulum vesicles due to the outflow of water. The following decrease in the light scattering intensity is caused by the increase of the volume due to the inflow of the solutes and water. From the former and the latter rates, the permeation times of water and the solutes could be calculated, respectively. According to the same method, permeation times of various salts were determined. The rate of the inflow of the salts was dependent on the movement of the slower ions, that is, ions move as a pair. In the case of potassium salts, an increase in the permeation rate of the salts was observed when valinomycin was added to the membrane suspensions. From these experiments, as a measure of permeability, half permeation times of various ions and molecules were determined. The following are typical results: water 0.1, Li+ 36, Na+ 26, K+20, Rb+ 16, Cl- 0.4, methanesulfonate 20, phosphate 10.5, oxalate 40 in seconds at room temperature. As a whole, sarcoplasmic reticulum was found to be an anion permeable membrane.

Animals↗
PubMedDate not supplied

[The calcium metabolism of myocardial mitochondria and sarcoplasmic reticulum in experimental potassium deficiency (author's transl)].

Mechanical Parameters of the whole, Langendorff-perfused cat heart and of isolated right ventricular papillary muscles are depressed in chronic potassium deficiency. 45Ca binding of sarcoplasmic reticulum (SR) was found to be diminished and correlated with a reduced contractility of the perfused hearts. 45Ca uptake of sarcoplasmic reticulum isolated from potassium deficient hearts was also reduced. The mitrochondrial 45Ca binding and endogenous Ca concentration were increased and there was a positive correlation between these two parameters. The data suggest that a reduced SR Ca binding plays a role in the depression of myocardial contractility in chronic potassium deficiency. Increased mitochondrial 45Ca binding in the presence of reduced 45Ca binding and uptake of sarcoplasmic reticulum suggests the possibility that mitochondria are an additional myocardial calcium pool in chronic potassium deficiency.

Animals↗
PubMed1975

Interactions of liver encoplasmic reticulum membranes and polysomes in vitro.

The interactions of various preparations of endoplasmic reticulum membranes and polysomes have been studied by means of a sandwich sucrose gradient that clearly isolates free ribosomes, smooth endoplasmic reticulum (S.E.R.) and rough endoplasmic reticulum (R.E.R.) from the microsomal fraction of rat liver homogenates. Reconstructed rough membranes separate well from the native R.E.R. but occupy the same position along the gradient as the S.E.R. and the rough membranes, stripped of their ribosomes by means of LiCl. Native R.E.R. and S.E.R. do not bind any added labeled polysomes at 0 degree C; previous treatment with LiCl does not modify the behavior of S.E.R. The presence of cell sap during the binding reaction does not increase polysome fixation by stripped-rough membranes but protects in some way the polysomes and preserves all their original functional capacity of amino acid incorporation into protein.

Animals↗
PubMed1978

Distension of the reticulum decreased food but not water intake by sheep.

The intakes of pelleted alfalfa by hungry sheep were depressed in a rectilinear manner in relation to the amount of water (0-800 ml) added to a balloon in the reticulum (p less than 0.005). Since the consumption of water by thirsty sheep was not altered by these treatments, the reduction in food intake produced by distending the reticulum was a specific response. The intakes of food were not significantly affected by distending the rumen with 800 ml water in a balloon so it is possible that the amount of fill in the reticulum rather than in the rumen may be important in signalling satiety in sheep.

Animals↗
PubMed1979

Electron probe X-ray microanalysis and cryoultramicrotomy of unstained myocardial sarcoplasmic reticulum, in situ and fragmented.

Myocardial sarcoplasmic reticulum of cats in situ and fragmented sarcoplasmic reticulum (FSR) were analysed using X-ray microanalysis, cryoultramicrotomy and scanning transmission electron microscopy. 2 types of FSR vesicles can be distinguished morphologically and by their different elemental composition especially by different Ca loading. The Ca content of the sarcoplasmic reticulum can also be detected in situ.

Animals↗
PubMed1978

Morphological aspects of some sodium transporting epithelia suggesting a transcellular pathway via elements of endoplasmic reticulum.

Electron microscopic studies of sodium transporting epithelia from frog skin, sheep choroid plexus, rabbit gallbladder and small intestine, and rat kidney revealed the presence of a complex intracellular system of tubulo-cisternal endoplasmic reticulum which appeared to connect apical (luminal) and baso-lateral cell surfaces. The system was present in the tight epithelium of frog skin but was most abundant in leaky epithelia with low transepithelial resistance and isotonic transport. The basic structural features of the system and its relationship with some associated components are described. Our result, coupled with preliminary physiological studies, indicate that developmental and seasonal (hormone-induced) changes in the configuration of the tubulo-cisternal endoplasmic reticulum may be closely correlated with specific changes in epithelial permeability. The findings are discussed in the light of the hypothesis that epithelia possess two sodium transporting systems: One based on pump sites in the plasma membrane producing a hypertonic transportate and another located in the membranes of the tubulo-cisternal endoplasmic reticulum which, due to its extensive surface, would be well suited for producing an isotonic transportate.

Animals↗
PubMed1982

Hypertrophic and hypoactive smooth endoplasmic reticulum in hepatocytes uremic patients. A morphometric and biochemical study.

Morphometric analysis of the hepatic endoplasmic reticulum and assays of drug-metabolizing enzymes in microsomes prepared from needle biopsy specimens were performed with samples from uremic patients on chronic hemodialysis and normal controls. The smooth endoplasmic reticulum (SER) morphometrically increased in the uremic patients, whereas the cytochrome P-450 content and the activity of p-nitroanisole O-demethylase per mg microsomal protein decreased in the uremic patients. This condition of SER corresponds to that of the so-called hypoactive hypertrophic smooth endoplasmic reticulum, which could suggest lower activity of hepatic microsomal drug oxidation in uremic patients. On the other hand, the P-450 content and the activity of p-nitroanisole O-demethylase per g liver were not significantly different between the uremic and the normal subjects. This seems to indicate that the capacity of drug oxidation is retained in whole livers of uremic patients. However, since some patients in this study showed markedly low activity of p-nitroanisole O-demethylase per mg microsomal protein and per g liver, lipophilic drugs metabolized in the liver as well as hydrophilic ones eliminated by the kidney should be carefully administered to uremic patients.

Adult↗
PubMed1993

Effects of selenium deficiency on Ca transport function of sarcoplasmic reticulum and lipid peroxidation in rat myocardium.

Two groups of weanling Sprague-Dawley rats were fed a low-selenium basal diet (Se 0.009 mg/kg) and the same diet supplemented with sodium selenite (Se 0.25 mg/kg), respectively, for 1, 2, and 3 months. At each feeding time, the Ca(2+)-ATPase activity, Ca2+ uptake rate and the capacity of Ca2+ uptake in isolated cardiac sacroplasmic reticulum from the Se-deficient rats were decreased significantly compared to those from the Se-supplemented rats, the contents of lipid peroxide in postmitochondrial supernatant and isolated sarcoplasmic reticulum from the Se-deficient rats were significantly higher than that from Se-supplemented rats. Compared to the Se-supplemented rats, the cytosolic glutathione peroxidase activity in Se-deficient rats decreased significantly. In addition, significant linear negative correlations of lipid peroxide in postmitochondrial supernatant to sarcoplasmic reticular Ca(2+)-ATPase activity, Ca2+ uptake rate and to whole blood selenium concentration were observed. The results suggest that the enhancement of lipid peroxidation via the depressed glutathione peroxidase activity might be responsible for the decrease of Ca(2+)-ATPase and Ca2+ uptake activities in sarcoplasmic reticulum in Se-deficient animals.

Animals↗
PubMed2000

Effect of carticaine on the sarcoplasmic reticulum Ca2+-dependent adenosine triphosphatase.

The sarcoplasmic reticulum Ca2+-ATPase (calcium-dependent adenosine triphosphatase) transports Ca2+ from the myoplasm to the reticulum lumen at the expense of free energy from ATP hydrolysis. Carticaine is a local anesthetic of frequent use in dentistry which is now entering other clinical fields. We studied the action of carticaine on the sarcoplasmic reticulum (SR) skeletal muscle Ca2+-ATPase. SR vesicles from rabbit fast skeletal muscle were used. Carticaine inhibits the enzymatic activity. The inhibition of the enzymatic activity depends on pH, [Ca2+] and the presence of calcimycin. Half-maximal carticaine concentration that inhibits the ATPase activity tends to a maximal value upon increasing [Ca2+]. Carticaine concentrations required to inhibit the enzymatic activity at myoplasmic calcium concentration are lower than usual clinical doses: Ki=6.0+/-1.4 mM carticaine (n=5) for 0.1 microM [Ca2+]. ATP-dependent calcium uptake is also inhibited by the local anesthetic: Ki=30.5+/-3.4 mM (n=4). Besides, carticaine inhibits the phosphorylation of the enzyme by inorganic phosphate (Pi): Ki=20.0+/-3.4 (n=5) - 33.2+/-4.6 (n=4) mM, for [Pi] 1-4 mM. Carticaine increases the membrane permeability to Ca2+. Ca2+ efflux from preloaded vesicles is prevented by Ca2+ and Mg2+. Our results suggest that the diffusion of the local anesthetic into muscle fibers might trigger undesired effects such as sustained contraction of the masticatory muscles.

Anesthetics, Local↗
PubMed2000

Protection of ischemic rat heart by dantrolene, an antagonist of the sarcoplasmic reticulum calcium release channel.

Cytosolic Ca2+ overload plays a major role in the development of irreversible injury during myocardial ischemia. Such overload is due at least in part to the release of Ca2+ from the sarcoplasmic reticulum. Therefore, we investigated whether dantrolene, a blocker of the sarcoplasmic reticulum Ca2+ release channel, may protect from ischemic injury. In binding experiments, we determined the effect of dantrolene on [3H]-ryanodine binding in rat cardiac tissue. In perfusion experiments, isolated rat hearts were perfused for 20 min in the working mode, in the presence of 0-45 microM dantrolene. The hearts were then subjected to 30 min of global ischemia and 120 min of retrograde reperfusion. Tissue injury was evaluated on the basis of triphenyltetrazolium chloride (TTC) staining and LDH release. The binding experiments showed that dantrolene displaced 4 nM [3H]-ryanodine with IC50 of 34 microM. In the perfusion experiments, tissue necrosis (i.e., TTC-negative tissue) averaged 28.3 +/- 1.6% of the ventricular mass under control conditions. Dantrolene was protective at micromolar concentrations: tissue necrosis decreased to 21.4 +/- 1.0% and 8.4 +/- 1.4% with 1 microM and 45 microM dantrolene, respectively (P < 0.05 and P < 0.01). Similar results were obtained with regard to LDH release. At low concentrations (up to 4 microM), dantrolene did not produce any significant hemodynamic effect, except for a slight increase in coronary flow, whereas at higher concentration a negative inotropic effect was apparent. In conclusion, dantrolene reduced ischemic injury even at concentrations that did not affect contractile performance. Modulation of sarcoplasmic reticulum Ca2+ release might represent a new cardioprotective strategy.

Animals↗
PubMed2003

Brefeldin A-regulated retrograde transport into the endoplasmic reticulum of internalised wheat germ agglutinin.

The effects of the fungal metabolite brefeldin A (BFA) on the endocytic routes of internalised wheat germ agglutinin (WGA) were studied in human HepG2 hepatoma cells, drawing particular attention to the application times in relation to the membrane dynamics occurring at the trans Golgi face during endocytosis. As shown in previous studies, transport of internalised WGA into the Golgi apparatus can be classified in three stages being characterised by predominance of vesicular endosomes (stage I), formation of an extended endocytic trans Golgi network (stage II) and uptake of WGA into the stacked Golgi cisternae (stage III). BFA treatment of the cells led to rapid tubular-reticular transformations of the Golgi stacks. Retrograde transport and further destinations of internalised WGA depended on the time of BFA application. When BFA was administered during stages I or II, WGA was localised within the BFA-induced tubules and networks, but never was found within the endoplasmic reticulum. By contrast, BFA treatment during stage III led to a redistribution of internalised WGA into cisternae of the endoplasmic reticulum. These results show that BFA administered according to a precise time schedule can be used as a regulatory agent that allows to control retrograde traffic of internalised molecules into the endoplasmic reticulum.

Biological Transport↗