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PubMed1996

[The reaction of the cytoskeleton and smooth endoplasmic reticulum of Mauthner's neurons in goldfish to partial denervation and prolonged sensory stimulation].

Structure of smooth endoplasmic reticulum and cytoskeleton of goldfish Mauthner neurons were studied together with the behavior of fish after partial deafferentation of one of the dendrites with following long-term natural stimulation of another one and soma. Strong disturbance of cytoskeleton and proliferation of smooth endoplasmic reticulum especially of its transversely localised component accompanies exhaustion of Mauthner neurons caused by stimulation in normal absolute afferentation. On behavioral level it is manifests in significant suppression of fish motor activity. Similar stimulation of partly deafferentated Mauthner neurons turns to be more sparing both for fish behaviour and Mauthner neurons structure. Proliferation of endoplasmic reticulum was not in fact observed and in the cytoskeleton bundles of filaments were detected which implies improvement of its physico-chemical characteristics and increase of resistance to external factors. Probably, this relative resistance of partly deafferentated Mauthner neurons of fish to long-term natural stimulation is conditioned predominantly by postsynaptic mechanisms and is likely linked with reorganization in cytoskeleton, caused by preliminary change of Mauthner neurons innervation.

Animals↗
PubMed1996

Conformational changes of smooth endoplasmic reticulum induced by brief anoxia in rat Purkinje cells.

Morphological changes of the smooth endoplasmic reticulum (SER) in rat cerebellar Purkinje cell dendrites were examined under apneic conditions for 1-5 minutes, induced by an incision of the diaphragm and the collapse of the lungs. The dendrites obtained from control rats contained a tubular network of the SER and hypolemmal cisterns adjacent to the plasma membrane. After a 3-5-minute apnea, the cytoplasm was occupied by many flattened cisterns stacked into lamellae, referred to as "lamellar bodies." A quantitative analysis revealed that the number of lamellar bodies became maximum after 3 minutes of apnea. After the treatment time, they increased in size by adding new cisterns to the previous core lamellae. This analysis also showed that the total amount of the SER membranes contained in a dendrite did not change during anoxia. Conformational changes from the tubular or hypolemmal SER to lamellar bodies during brief anoxia might occur through a transient and intermediate form of "fenestrated cisterns," flat across the transverse plane and penetrated by many longitudinally arranged microtubules. We suggest that these morphological changes of the SER during brief anoxia are not fixation artifacts but represent a biological reaction for protecting against intracellular abnormalities during anoxia.

Animals↗
PubMed1982

The production of smooth endoplasmic reticulum and formation of an abnormal amorphous material by the immature 5-day-old chick hepatocytes in culture under the influence of phenobarbital.

The experiment was performed to see if the 5-day-old chick hepatocytes which normally do not produce smooth endoplasmic reticulum in culture, would do so under the influence of phenobarbital. The results indicated that under the influence of phenobarbital, the 5-day hepatocyte produces a small amount of smooth endoplasmic reticulum. However, a more significant observation is that the 5-day-old hepatocytes in the presence of phenobarbital also produce a large amount of amorphous material which is deposited in circumscribed areas of the cytoplasm. It appears that the amorphous material is initially deposited into the cisternal space of the rough endoplasmic reticulum which dilates and the membrane fragments to release the amorphous substance into the cytoplasm. The 5-day-old chick hepatocytes produce a lot more amorphous material than the 11-day-old cells, which formed so little. If, as suggested by many authors (Banjo & Nemeth, 1976; Ernster & Orrenius, 1965; Orrenius, 1965; Orrenius, Ericsson & Ernster, 1965, some of the enzymes produced as a result of the stimulation of the cells by phenobarbital are inseparably located on the membranes of the endoplasmic reticulum (RER and SER), i.e. the enzymes are only stable when attached to the membrane, it may be that the large amount of enzymes produced by the hypertrophied rough and endoplasmic reticulum (Banjo & Nemeth, 1976) in the 5-day-old hepatocytes in culture under the influence of phenobarbital could not find enough smooth endoplasmic reticulum membrane for attachment in the same 5-day-old cells whose capacity for producing smooth endoplasmic reticulum is very limited. Therefore, this large amount of enzyme and the few membranes are not organized and are therefore liberated, as the amorphous material, into the cytoplasm. The 11-day-old hepatocytes, on the other hand, formed very little amorphous material, and this may be due to its high capacity to make smooth endoplasmic reticulum membranes. It is suggested that the large amount of amorphous material liberated in the 5-day-old cells represents the unorganized enzymes and membranes.

Animals↗
PubMed2001

A role for smooth endoplasmic reticulum membrane cholesterol ester in determining the intracellular location and regulation of sterol-regulatory-element-binding protein-2.

Cellular cholesterol homoeostasis is regulated through proteolysis of the membrane-bound precursor sterol-regulatory-element-binding protein (SREBP) that releases the mature transcription factor form, which regulates gene expression. Our aim was to identify the nature and intracellular site of the putative sterol-regulatory pool which regulates SREBP proteolysis in hamster liver. Cholesterol metabolism was modulated by feeding hamsters control chow, or a cholesterol-enriched diet, or by treatment with simvastatin or with the oral acyl-CoA:cholesterol acyltransferase inhibitor C1-1011 plus cholesterol. The effects of the different treatments on SREBP activation were confirmed by determination of the mRNAs for the low-density lipoprotein receptor and hydroxymethylglutaryl-CoA (HMG-CoA) reductase and by measurement of HMG-CoA reductase activity. The endoplasmic reticulum was isolated from livers and separated into subfractions by centrifugation in self-generating iodixanol gradients. Immunodetectable SREBP-2 accumulated in the smooth endoplasmic reticulum of cholesterol-fed animals. Cholesterol ester levels of the smooth endoplasmic reticulum membrane (but not the cholesterol levels) increased after cholesterol feeding and fell after treatment with simvastatin or C1-1011. The results suggest that an increased cellular cholesterol load causes accumulation of SREBP-2 in the smooth endoplasmic reticulum and, therefore, that membrane cholesterol ester may be one signal allowing exit of the SREBP-2/SREBP-cleavage-regulating protein complex to the Golgi.

Acetamides↗
PubMed1981

Effects of glucagon on hepatic glycogen and smooth endoplasmic reticulum.

The action of glucagon on hepatic glycogen and smooth endoplasmic reticulum (SER) was studied in samples of liver taken sequentially from anesthetized rats. The physiological state of each animal was assessed by continuously monitoring aortic blood pressure and blood lactatepyruvate ratios. High hepatic glycogen levels were established by using 10--12 hr fasted control-fed rats infused continuously with glucose. In rats receiving glucose only, hepatic glycogen levels remained above 5.0% during the 4-hr period of glucose administration. Centrilobular hepatocytes displayed an abundance of glycogen which often appeared dispersed with elements of SER between the glycogen particles. Periportal cells had dense clumps of glycogen with few vesicles of SER restricted to the periphery of the glycogen masses. The addition of glucagon to the glucose infusate caused a marked stimulation of glycogenolysis. In these rats, the hepatic glycogen level (X +/- SE) was 6.74 +/- .15% 1 hr after glucose and declined after initiation of glucagon infusion as follows: 5.86 +/- .29% (15 min), 4.89 +/- .26% (1 hr), 2.16 +/- .40% (2 hr), and 1.66 +/- .29% (3 hr). The fine structure of hepatocytes showed a dramatic response to the administration of glucagon. The glycogen regions of the cells were noticeably decreased in size and number of glycogen granules 3 hr after initiation of glucagon infusion, and SER was abundant in both periportal and centrilobular hepatocytes. The interpretation offered is that glucagon induces the formation of new SER membranes which participate in glycogen breakdown and/or glucose release from hepatocytes.

Animals↗
PubMed1980

Intracellular distribution of Sindbis virus membrane proteins in BHK-21 cells infected with wild-type virus and maturation-defective mutants.

The association of Sindbis virus proteins with cellular membranes during virus maturation was examined by utilizing a technique for fractionating the membranes of BHK-21 cells into three subcellular classes, which were enriched for rough endoplasmic reticulum, smooth endoplasmic reticulum, and plasma membrane. Pulse-chase experiments with wild-type (strain SVHR) virus-infected cells showed that virus envelope proteins were incorporated initially into membranes of the rough endoplasmic reticulum and subsequently migrated to the smooth and plasma membrane fractions. Large amounts of capsid protein were associated with the plasma membrane fraction even at the earliest times postpulse, and relatively little was found associated with the other membranes, suggesting a rapid and preferential association of nucleocapsids with the plasma membrane. We also examined the intracellular processing of the proteins of two temperature-sensitive Sindbis virus mutants in pulse-chase experiments at the nonpermissive temperature. Labeled virus proteins of mutant ts-20 (complementation group E) first appeared in the rough endoplasmic reticulum and were then transported to the smooth and plasma membrane fractions, as in wild-type (strain SVHR) virus-infected cells. In cells infected with ts-23 (complementation group D), the pulse-labeled virus proteins appeared initially in the rough membrane fraction and were transported to the smooth membrane fraction, but only limited amounts reached the plasma membrane. Thus, in ts-23-infected cells, the transport of the virus-encoded proteins from the smooth membranes seemed to be defective. In both ts-20- and ts-23-infected cells the envelope precursor polypeptide PE2 was not processed to E2, and no label was incorporated into free virus at the nonpermissive temperature.

Animals↗
PubMed2003

[Myelin-like structures as a possible source of the smooth endoplasmic reticulum in early amphibian oocytes].

A comparative study of amphibian oocyte ultrastructural organization has shown a significant accumulation of elements of the smooth endoplasmic reticulum in the oocyte cytoplasm at the third stage of development. The analysis of oocytes of two frog species, Xenopus laevis and Rana temporaria, at the first and second stages of their development enabled us to recognize in the cytoplasm of the oocyte some myelin-like structures (MLs) made of 30-40 densely packaged membranous layers and shaped as dense bodies. MLs are also present in the adjacent follicular cells and in the intercellular space. In the oocyte cytoplasm these structures are located near the nuclear envelope and other intracellular organelles. At the third stage of oogenesis, which is characterized by a high functional activity of the cells, MLs are seen to unwrap sequentially into double-layer membranes similar to the smooth endoplasmic reticulum cisternae. Intermediate steps of this process being also observed. It is supposed that MLs may play the role of membrane stocks to be used eventually for the formation of nascent endoplasmic membranes in the amphibian oocytes.

Animals↗
PubMed1985

Epoxide hydrolase is a marker for the smooth endoplasmic reticulum in rat liver.

Epoxide hydrolase (EH, EC 3.3.2.3) was chosen as a potential marker for smooth endoplasmic reticulum, because this enzyme is inducible by drugs such as phenobarbital. The hypothesis was verified in rat liver using immunochemical and immunocytochemical techniques. Antibodies were raised to the purified protein. These antibodies were affinity purified using the enzyme immobilized on Sepharose Ultrogel. The specificity of the antibodies was assayed by immunoelectrotransfer (Western blot). The labelling of rat liver thin frozen sections with protein A-gold particles demonstrated that the antibodies specifically recognised smooth endoplasmic reticulum membranes. Rough endoplasmic reticulum, other intracellular organelles and plasma membrane were unlabelled.

Animals↗
PubMed2000

Inositol trisphosphate and cyclic adenosine diphosphate-ribose increase quantal transmitter release at frog motor nerve terminals: possible involvement of smooth endoplasmic reticulum.

The release of chemical transmitter from nerve terminals is critically dependent on a transient increase in intracellular Ca2+. The increase in Ca2+ may be due to influx of Ca2+ from the extracellular fluid or release of Ca2+ from intracellular stores such as mitochondria. Whether Ca2+ utilized in transmitter release is liberated from organelles other than mitochondria is uncertain. Smooth endoplasmic reticulum is known to release Ca2+, e.g., on activation by inositol trisphosphate or cyclic adenosine diphosphate-ribose, so the possibility exists that Ca2+ from this source may be involved in the events leading to exocytosis. We examined this hypothesis by testing whether inositol trisphosphate and cyclic adenosine diphosphate-ribose modified transmitter release. We used liposomes to deliver these agents into the cytoplasmic compartment and binomial analysis to determine their effects on the quantal components of transmitter release. Administration of inositol trisphosphate (10(-4)M) caused a rapid, 25% increase in the number of quanta released. This was due to an increase in the number of functional release sites, as the other quantal parameters were unaffected. The effect was reversed with 40 min of wash. Virtually identical results were obtained with cyclic adenosine diphosphate-ribose (10(-4)M). Inositol trisphosphate caused a 10% increase in quantal size, whereas cyclic adenosine diphosphate-ribose had no effect. The results suggest that quantal transmitter release can be increased by Ca2+ released from smooth endoplasmic reticulum upon stimulation by inositol trisphosphate or cyclic adenosine diphosphate-ribose. This may involve priming of synaptic vesicles at the release sites or mobilization of vesicles to the active zone. Inositol trisphosphate may have an additional action to increase the content of transmitter within the vesicles. These findings raise the possibility of a role of endogenous inositol phosphate and smooth endoplasmic reticulum in the regulation of cytoplasmic Ca2+ and transmitter release.

Adenosine Diphosphate Ribose↗
PubMed1968

Hypertrophic, hypoactive smooth endoplasmic reticulum: a sensitive indicator of hepatotoxicity exemplified by dieldrin.

Rats with hypertrophic smooth endoplasmic reticulum (ER) and increased activities of the drug-handling enzymes induced by dieldrin were stressed with larger doses of the pesticide. The activity of the drug-handling enzymes was thus reduced, but liver weight, smooth ER, and P-450 hemoprotein remained elevated. While no changes were apparent by light microscopy, the hypertrophic, hypoactive smooth ER was recognized as tight clusters of tubular membranes associated with abnormalities of the mitochondrial membrane. Similar but not identical morphologic changes were noted in human liver diseases associated with hepatic insufficiency. Hypertrophic, hypoactive smooth ER may indicate transition from adaptation of injury, and can be used as a sensitive parameter of toxicity.

Animals↗
PubMed1996

The association of phosphorylase kinase with membranes of rat liver smooth endoplasmic reticulum.

Upon fractionation of a post mitochondrial supernatant from rat liver, phosphorylase kinase activity was largely recovered in the cytosol and the smooth endoplasmic reticulum (SER) fraction. The presence of phosphorylase kinase in SER vesicles was not due to an interaction of the enzyme with glycogen particles, since previous elimination of SER glycogen either by 48 h animal starvation or by treatment of the membrane fraction with alpha-amylase did not significantly alter phosphorylase kinase activity content. Washing of the initial pellet of SER fraction (crude SER) by dilution and recentrifugation, released in the supernatant an amount of phosphorylase kinase activity, which is dependent on: i) the degree of dilution, ii) the number of washes, iii) the ionic strength of the washing solution and iii) the presence or absence of Ca2+. Crude SER-associated phosphorylase kinase was marginally affected by increased concentrations of antibody against rabbit skeletal muscle holoenzyme which nevertheless drastically inhibited cytosolic enzyme activity, while it showed a higher resistance to partial proteolysis and a different Western blotting profile with anti-phosphorylase kinase when compared with the soluble kinase. A small but significant fraction of SER phosphorylase kinase was strongly associated with the microsomal fraction being partly extractable only in presence of detergents. This membrane-bound enzyme form exhibited an alkaline pH optimum, in contrast to the neutral pH optima of both soluble and weakly associated phosphorylase kinase.

Animals↗
PubMedDate not supplied

Adrenergic nerve smooth endoplasmic reticulum calcium buffering declines with age.

Calcium buffering capacity declines with age in sympathetic nerves of rat tail artery. To test whether smooth endoplasmic reticulum (SER) calcium buffering declines with age, effects of two SER calcium-ATPase inhibitors on norepinephrine release and intracellular calcium were determined. Thapsigargin or cyclopiazonic acid caused a significant increase in stimulation-evoked norepinephrine release from 6 month tail arteries with much less effect in 20 months. In isolated superior cervical ganglion cells, the rate of rise of calcium with K+-depolarization increased only in young cells with either cyclopiazonic acid or thapsigargin, with no effect in the old. In young cells, cyclopiazonic acid significantly influenced time to peak, rate of decline, and time to basal of K+-evoked calcium transients, but had no effect in old cells. Thapsigargin caused a significant increase in rate of decline in young, but not old, cells. These differential effects suggest an age-related decline in function of SER calcium buffering mechanisms in the sympathetic nervous system causing older nerves to become more reliant on mitochondria to buffer calcium.

Adenosine Triphosphatases↗
PubMedDate not supplied

Morphologic features of the liver in abetalipoproteinemia.

Liver tissue of a newly diagnosed 30-year-old patient with abetalipoproteinemia was studied by light and electron microscopy. Despite accumulation of large quantities of lipid droplets in hepatocytes, the lobular architecture remained intact, and there was no fibrosis. Acanthocytes were readily identified in sinusoids by scanning electron microscopy. Profiles of rough endoplasmic reticulum, smooth endoplasmic reticulum and Golgi apparatus appeared normal by transmission electron microscopy. Lipid droplets were not bound to membranes and were not associated with the endoplasmic reticulum or Golgi apparatus. In abetalipoproteinemia, these morphological features are consistent with defective apolipoprotein B synthesis. This prevents assembly of lipoproteins that can be secreted through the normal intracellular communicating tubular network and, consequently, fat accumulates in the cytoplasm of the hepatocytes.

Abetalipoproteinemia↗
PubMed1977

Fine structure of seminiferous tubules in antarctic seals.

The fine structure of seminiferous tubules from 5 crabeater, 2 leopard and 2 Ross seals showed that during the nonbreeding season the tubules were essentially similar in possessing spermatogenic and Sertoli cells. However, the tubules of leopard and Ross seals had more primary and secondary spermatocytes and spermatids than the crabeater seals. In general, the tubules were devoid of spermatozoa. The spermatids showed stages of maturation such as Golgi phase of acrosome formation, acrosomal cap formation and condensation of nuclei. Some spermatids degenerated in tubules. Both maturing and degenerating spermatids were closely associated with Sertoli cells. Junctional complexes with plaques of filaments were observed between Sertoli cells and the spermatogenic cells. Sertoli cells, irregular and polygonal, contained highly convoluted nuclei, strands of rough endoplasmic reticulum, smooth endoplasmic reticulum, Golgi complexes, small mitochondria, variable amounts of lipid droplets, lysosomes, lipofuscin granules and highly plicated plasma membranes. In brief, the spermatogenic activity had practically ceased in the testes and the animals probably secreted low levels of testosterone during the nonbreeding season.

Animals↗
PubMed1975

Stimulation of the adrenal gland of the Mongolian gerbil after ovariectomy.

The effect of ovariectomy on the adrenal gland was studied in the Mongolian gerbil. Castration stimulated cells in the zona fasciculata as well as those in the region between the zona fasciculata and zona reticularis. No alterations occurred in the zona reticularis. The width of the intermediate region was enlarged, the cells were hypertrophic and contained an increased number of concentric whorls of rough endoplasmic reticulum. Smooth endoplasmic reticulum was hypertropic in cells of the zona fasciculata and intermediate region. Many mitochondria in cells of the intermediate region were larger than those in controls. Stimulation of cellular ultrastructure is directly correlated with a significant elevation in plasma cortisol in ovariectomized gerbils.

Adrenal Cortex↗