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Results for “Cytoplasmic Streaming”

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PubMed1979

Proposal of a a neurosecretory system in the pancreas. An electron microscope study in the dog.

The nerve fibers supplying the islets of the dog pancreas were examined by electron microscopy. Axons with swollen portions containing various types of synaptic vesicles, including a cholinergic type, two varieties of presumable aminergic type and a possible peptidergic type, rush to the pericapillary space to end there, whereas only a small part of them seem to terminate on the endocrine cells of the islet. Schwann cell cytoplasm invests the axons and often separates these from the endocrine cells. The terminal portions filled with vesicles usually become free of the Schwann sheath on the side facing the blood capillary. Here the neuronal secretions are believed to be released into the blood stream through the pored endothelium of the capillary. The neurosecretions, together with the islet hormones are distributed to the exocrine pancreas in high concentrations via the insulo-acinar portal system. It seems thus sufficient for the nerves to supply the islet in order to control the exocrine function of the pancreas.

Animals↗

PubMed1990

Canine X-linked muscular dystrophy: morphologic lesions.

Gross pathologic lesions and light microscopic and ultrastructural features of skeletal muscle lesions in canine X-linked muscular dystrophy (CXMD) were studied in dogs from 3 months to 6 years of age. Necrosis and regeneration were present at all ages, but were most prominent in the youngest dogs studied. Increased intracytoplasmic calcium, as evidenced by positive alizarin red S staining, was associated with fiber necrosis, but was also seen in small numbers of otherwise normal fibers. Progressive changes included development of severe fiber size variation, endomysial and perimysial fibrosis, prominent cytoplasmic disorganization, internalization of myonuclei, mitochondrial proliferation, mild fat infiltration, and alterations in the fiber-type pattern. The most consistent early ultrastructural changes were dilatation of the sarcoplasmic reticulum and focal subsarcolemmal areas of degeneration. Convincing sarcolemmal defects were not found. Z-band streaming was present at all ages, and Z-band duplication and nemaline rods were seen in older dogs. Evidence for abnormal regeneration was found in the oldest dog, and was associated with extensive fibrosis. These findings document the progression of lesions in CXMD, and illustrate the profound alterations in fiber organization and fiber type that may occur in late stages of dystrophin-deficient muscular dystrophy.

Aging↗

PubMed2002

Characterization and functional analysis of the siderophore-iron transporter CaArn1p in Candida albicans.

Siderophores are small organic compounds with high affinity for ferric iron. Microorganisms commonly acquire iron via siderophore secretion and uptake. Here we report the characterization of the siderophore transporter CaArn1p in the fungal pathogen Candida albicans. Deletion of CaARN1 reduced the ability of C. albicans to use iron bound to the hydroxamate-type siderophore ferrichrome and abolished it when two high-affinity iron permease genes (CaFTR1 and CaFTR2) were also deleted, indicating a role of CaArn1p as well as the permeases in ferrichrome-iron uptake. Caarn1Delta (but not Caftr1DeltaCaftr2Delta) assimilated iron from another hydroxamate-type siderophore, ferrioxamine B, suggesting that iron uptake from this compound depends on the permeases, but not on CaArn1p. Northern blot analysis revealed that the transcription repressor CaTup1p repressed CaARN1 expression under iron-replete conditions via the DNA-binding protein Rfg1p. Green fluorescent protein-tagged CaArn1p was observed predominantly in the plasma membrane, with some in the cytoplasm as distinct spots. The number of these spots increased with the increase in ferrichrome concentration, suggesting that CaArn1p internalization might be a mechanism for ferrichrome-iron uptake or for recycling the transporter. Caarn1Delta did not show reduced virulence when injected into the blood stream of mice, implying that CaArn1p is not required for iron uptake along this route of infection.

Animals↗

PubMed2001

Xenopus cadherin-11 restrains cranial neural crest migration and influences neural crest specification.

Cranial neural crest (CNC) cells migrate extensively, typically in a pattern of cell streams. In Xenopus, these cells express the adhesion molecule Xcadherin-11 (Xcad-11) as they begin to emigrate from the neural fold. In order to study the function of this molecule, we have overexpressed wild-type Xcad-11 as well as Xcad-11 mutants with cytoplasmic (deltacXcad-11) or extracellular (deltaeXcad-11) deletions. Green fluorescent protein (GFP) was used to mark injected cells. We then transplanted parts of the fluorescent CNC at the premigratory stage into non-injected host embryos. This altered not only migration, but also the expression of neural crest markers. Migration of transplanted cranial neural crest cells was blocked when full-length Xcad-11 or its mutant lacking the beta-catenin-binding site (deltacXcad-11) was overexpressed. In addition, the expression of neural crest markers (AP-2, Snail and twist) diminished within the first four hours after grafting, and disappeared completely after 18 hours. Instead, these grafts expressed neural markers (2G9, nrp-I and N-Tubulin). Beta-catenin co-expression, heterotopic transplantation of CNC cells into the pharyngeal pouch area or both in combination failed to prevent neural differentiation of the grafts. By contrast, deltaeXcad-11 overexpression resulted in premature emigration of cells from the transplants. The AP-2 and Snail patterns remained unaffected in these migrating grafts, while twist expression was strongly reduced. Co-expression of deltaeXcad-11 and beta-catenin was able to rescue the loss of twist expression, indicating that Wnt/beta-catenin signalling is required to maintain twist expression during migration. These results show that migration is a prerequisite for neural crest differentiation. Endogenous Xcad-11 delays CNC migration. Xcad-11 expression must, however, be balanced, as overexpression prevents migration and leads to neural marker expression. Although Wnt/beta-catenin signalling is required to sustain twist expression during migration, it is not sufficient to block neural differentiation in non-migrating grafts.

Animals↗

PubMed2006

S-adenosylhomocysteine hydrolase is localized at the front of chemotaxing cells, suggesting a role for transmethylation during migration.

Chemotaxis of bacteria requires regulated methylation of chemoreceptors. However, despite considerable effort in the 1980s, transmethylation has never been established as a component of eukaryotic cell chemotaxis. S-adenosylhomocysteine (SAH), the product formed when the methyl group of the universal donor S-adenosylmethionine (SAM) is transferred to an acceptor molecule, is a potent inhibitor of all transmethylation reactions. In eukaryotic cells, this inhibition is relieved by hydrolysis of SAH to adenosine and homocysteine catalyzed by SAH hydrolase (SAHH). We now report that SAHH, which is diffuse in the cytoplasm of nonmotile Dictyostelium amoebae and human neutrophils, concentrates with F-actin in pseudopods at the front of motile, chemotaxing cells, but is not present in filopodia or at the very leading edge. Tubercidin, an inhibitor of SAHH, inhibits both chemotaxis and chemotaxis-dependent cell streaming of Dictyostelium, and chemotaxis of neutrophils at concentrations that have little effect on cell viability. Tubercidin does not inhibit starvation-induced expression of the cAMP receptor, cAR1, or G protein-mediated stimulation of adenylyl cyclase activity and actin polymerization in Dictyostelium. Tubercidin has no effect on either capping of Con A receptors or phagocytosis in Dictyostelium. These results add SAHH to the list of proteins that redistribute in response to chemotactic signals in Dictyostelium and neutrophils and strongly suggest a role for transmethylation in chemotaxis of eukaryotic cells.

Actins↗

PubMed2004

The unique C-terminal tail of the mitogen-activated protein kinase ERK5 regulates its activation and nuclear shuttling.

ERK5 is unique among mitogen-activated protein kinases (MAPKs) in that it contains a large C-terminal tail. We addressed the question of how this tail could affect the signaling capacity of ERK5. Gradual deletion of the C-terminal domains resulted in a drastic increase of ERK5 kinase activity, which was dependent on the up-stream MAPK cascade, thus indicating a possible auto-inhibitory function of the tail. It is interesting that ERK5 was able to autophosphorylate its own tail. Moreover, ERK5, which was found to be expressed in virtually all kinds of cell lines, localized to nuclear as well as cytoplasmic compartments. The localization of ERK5 was determined by its C-terminal domains, which were also required for appropriate nucleocytoplasmic shuttling. Taken together, these results indicate that ERK5 signaling is directed by the presence of its unique C-terminal tail, which might be the key to understanding the key role of ERK5 in MAPK signaling.

Active Transport, Cell Nucleus↗

PubMed1994

[Influence of ceruloplasmin on the embryotoxic effect of silver ions].

The effect of alimentary administration of silver salts upon embryogenesis in rats has been studied. Feeding of AgCl to pregnant female rats throughout gestation did not result in any alterations in their physiological functions, although the active copper-containing ceruloplasmin (Cp) was eliminated from the blood stream. However, anomalous development of embryos, their prenatal death or total mortality of newborn rats within the first 24 hours after birth were evidenced. The copper content in the placenta and embryonic tissues decreased appreciably. The Cu,Zn-superoxide dismutase (SOD) activity was diminished in the cytoplasm of embryonic cells alongside with its drop, though less pronounced, in the tissues of the pregnant females. The embryotoxicity of AgCl was considerably reduced by repetitive injections of native Cp to pregnant rats. Such treatment caused an increase in the SOD activity in the placenta and embryonic tissues. Mortality of the newborns also went down. It is suggested that the embryotoxic effect of AgCl is due to its ability to interfere with copper metabolism, by altering the copper-transporting function of Cp.

Animals↗

PubMed1981

Early glomerular lesions in amyloidosis. Electronmicroscopic findings.

Our investigations on early glomerular changes in renal amyloidosis showed the following: 1. In some renal biopsies, amyloid was demonstrated in the mesangial matrix predominantly and could be seen penetrating through the basement membrane of the mesangial region into the subepithelial space of adjacent glomerular capillaries. 2. In other biopsies, showing the same severity of amyloidosis, deposits were demonstrated in the mesangium and in the capillary walls distant from the mesangium on both sides of the basement membrane. There was no apparent connection between the deposits in these two areas. 3. On the basis of the morphological changes found in the cytoplasm of the mesangial cells, the glomerular epithelial cells and partly also in the endothelial cells, supported by our electron microscopic findings in the immediate vicinity of these cells, we come to the conclusion that amyloid in the glomerulus is formed from amyloid precursors brought via the blood stream. 4. Amyloid fibrils may be formed in the extracellular space of the glomerulus under the influence of lysosomal enzymes released from epithelial, mesangial and perhaps endothelial cells, by action of these enzymes on extracellularly deposited amyloid precursors.

Amyloidosis↗

PubMed2004

Efficacy of boron neutron capture therapy on liver metastases of colon adenocarcinoma: optical and ultrastructural study in the rat.

The effect of neutron boron capture therapy (BNCT) was studied in rat tumor liver cells after induction of the liver metastases by splenic inoculation of cells from DHA/K12/TRb line. Ten days following the treatment, the BPA was injected into rats and therefore the animals were sacrificed, the liver was exposed to neutron irradiation and processed. In some experiments the liver was reimplanted (after irradiation) in syngenic animals and studied 3 days later, following sacrifice. Samples of tissue obtained from metastasised and non-metastasised areas of the liver parenchyma, before and after the neutron irradiation, were examined in light microscopy and electron microscopy. The analysis pointed out damages induced by the neutron treatment in single tumor cells mostly localised in the synusoidal blood stream. Debris and apoptotic cells were sometimes observed in the neoplastic nodules before treatment, while the tumor cell death (apoptosis) increased in the tumor cells following BNCT treatment. An intense scavenger activity of Kupffer cells after irradiation was accompanied by a strong acid phosphatase reaction detectable in wide cytoplasmic areas. In the liver parenchyma of reimplanted animals, the presence of large collagen bundles spread among the hepatocytes was observed at electron microscopy.

Adenocarcinoma↗

PubMed1981

BCG-induced changes in the post capillary venules of the guinea pig lymph node.

The post capillary venules (PCV) of the regional lymph nodes of BCG-injected male and female guinea pigs were examined under light and electron microscopy. The endothelial cells showed increased height and pyroninophilia. Their cytoplasm contained increased numbers of ribosomes and polyribosomes and prominent rough endoplasmic reticulum with occasionally dilated cisternae. The number of lymphocytes migrating through the PCV wall was also increased. The activation of the endothelial cells of PCV induced by BCG may increase the recirculation of lymphocytes from the blood stream. These may be of importance in the antitumour activity of BCG. In control guinea pigs the height of the endothelial cells of PCV was significantly greater in the female than in the male. After BCG injection this sex difference was still apparent.

Animals↗

PubMed1976

[Effect of temporary ischemia with subsequent recirculation on the ultrastructure of glomerular capillaries and nephrons].

The influence of temporary ischemia followed by recirculation on the ultrastructure of glomerular capillaries and some portions of the nephron was studied in 20 albino rats which were subjected to compression of the vascular bundle of the left kidney for 30 min., 1, 2 and 3 hours followed by recovery of the blood stream in the ischemic organ for 3 hours (with a simultaneous nephrectomy of the right kidney). The electron microscopic analysis has established that the amount of micropinocytic vesicles become markedly increased within 3 hours following 30-min. ischemia of the kidney with the recovery of blood circulation in the cytoplasm of endotheliocytes of glomerular blood capillaries. With increased terms of the left kidney ischemia (1, 2, 3 hs) the ultrastructural changes in endotheliocytes increased. There appeared microclasmatosis of the internal plasmalemma of endotheliocytes, the flattened peripheral part of the cytoplasm underwent considerable destruction. Swelling of microvilli of the brush border and vacuolization of the cytoplasm were observed in nephrocytes of the proximal part of the nephron in short-term ischemia (30 min) followed by the recovery of circulation for 3 hours. Longer periods of ischemia (1, 2, 3 hs) casued destruction of the brush border. There appeared secondary lysosomes, in mitochondria there occurred discomplexation and lysis of cristae.

Acute Disease↗

PubMed1980

Glycosaminoglycan distribution in rabbit aortic wall following balloon catheter deendothelialization. An ultrastructural study.

The glycosaminoglycan (GAG), content of rabbit aortic wall was assayed morphometrically using ruthenium red-stained sections viewed by transmission electron microscopy. Two types of ruthenium red-positive granules were identified in the intercellular matrix. Large granules (20 to 50 nm. in diameter) with interconnecting fibrils were removed by digestion of the tissue with testicular hyaluronidase or chondroitinase ABC. Smaller granules (20 nm). were localized mainly in endothelial basement membrane and were resistant to digestion by these enzymes. Both types of granules were removed from the tissue by the action of nitrous acid. At intervals of 11 to 17 weeks after a single balloon deendothelialization of the aortas of normolipemic rabbits, there were significantly more granules of both types in areas where endothelium had regenerated over the neointima than in areas not covered by endothelium. Lipid also accumulated preferentially in the endothelium-covered neointima. Compared to normal aortas, there is an increase in the large granule content in the reendothelialized areas and a decrease in both large and small granule content in the nonendothelialized areas. It is suggested that GAG may trap low density lipoproteins. The low GAG content of the nonendothelialized neointima may account for the low lipid content; additionally, the lack of endothelial cover may allow diffusion of GAG out of these areas carrying low density lipoprotein into the blood stream in the form of GAG-low density lipoprotein complexes or low density lipoprotein removal may be facilitated by high density lipoprotein.

Animals↗

PubMed1980

Studies on microplasmodia of Physarum polycephalum. I. Classification and locomotion behavior.

Depending on the conditions of the axenic shuttle culture, microplasmodia of the acellular slime mold Physarum polycephalum can be subdivided into three classes regarding fine structural organization and protoplasmic streaming activity: (1) spherical and rod-shaped types, (b) ameboid types, and (c) symmetrical types. In ameboid microplasmodia, the motive force for the irregular protoplasmic streaming activity is generated by alternative contraction and relaxation of a membrane-associated layer, morphologically consisting exclusively of thin filaments (probably actin). The protoplasm flows along a hydraulic pressure gradient produced by the filament layer within limited regions of the cell periphery. In dumbbell-shaped microplasmodia the motive force for the regular protoplasmic shuttle streaming between the two spherical heads is generated both by volume changes of the peripheral cell region (caused by the contractile activity of the membrane-associated filament layer), and by volume changes of the internal cell membrane invagination system (caused by fibrils attached to the basal region of the invaginations). The development from the unordered protoplasmic streaming pattern and less complicated fine structural organization in ameboid microplasmodia to the highly organized protoplasmic shuttle streaming and the more complicated morphology in dumbbell-shaped microplasmodia can be explained by intermediate stages. Whereas the motive force for the transport of smaller amounts of protoplasm can be generated by the exclusive action of a cortical filament layer, the existence of a filament cortex, the display of cytoplasmic fibrils, and the development of plasma membrane invaginations appear to be a necessary precondition for the transport of large amounts of protoplasm.

Cytoplasm↗

PubMed1975

Ultrastructural features of degenerated cardiac muscle cells in patients with cardiac hypertrophy.

Degenerated cardiac muscle cells were present in hypertrophied ventricular muscle obtained at operation from 12 (38%) of 32 patients with asymmetric septal hypertrophy (hypertrophic cardiomyopathy) or aortic valvular disease. Degenerated cells demonstrated a wide variety of ultrastructural alterations. Mildly altered cells were normal-sized or hypertrophied and showed focal changes, including preferential loss of thick (myosin) filaments, streaming and clumping of Z band material, and proliferation of the tubules of sarcoplasmic reticulum. Moderately and severely degenerated cells were normal-sized or atrophic and showed additional changes, including extensive myofibrillar lysis and loss of T tubules. The appearance of the most severely degenerated cells usually reflected the cytoplasmic organelle (sarcoplasmic reticulum, glycogen, or mitochondria) which underwent proliferation and filled the myofibril-free areas of these cells. Moderately and severely degenerated cells were present in areas of fibrosis, had thickened basement membranes, and had lost their intercellular connections. These observations suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic ventricular hypertrophy.

Adolescent↗

PubMedDate not supplied

Calcium signaling in liver.

In hepatocytes, hormones linked to the formation of the second messenger inositol 1,4,5-trisphosphate (InsP3) evoke transient increases or spikes in cytosolic free calcium ([Ca2+]i), that increase in frequency with the agonist concentration. These oscillatory Ca2+ signals are thought to transmit the information encoded in the extracellular stimulus to down-stream Ca2+-sensitive metabolic processes. We have utilized both confocal and wide field fluorescence microscopy techniques to study the InsP3-dependent signaling pathway at the cellular and subcellular levels in the intact perfused liver. Typically InsP3-dependent [Ca2+]i spikes manifest as Ca2+ waves that propagate throughout the entire cytoplasm and nucleus, and in the intact liver these [Ca2+]i increases are conveyed through gap junctions to encompass entire lobular units. The translobular movement of Ca2+ provides a means to coordinate the function of metabolic zones of the lobule and thus, liver function. In this article, we describe the characteristics of agonist-evoked [Ca2+]i signals in the liver and discuss possible mechanisms to explain the propagation of intercellular Ca2+ waves in the intact organ.

Animals↗

PubMedDate not supplied

[Clinical aspects and diagnostic and therapeutic approaches to motor and sensory hereditary neuropathies (NHMS)].

INTRODUCTION: The classifications of peripheral neuropathies are continually being revised in the light of advances in genetic and biochemical investigation. OBJECTIVE: We establish a classification based on the pathology found in different anatomical structures of nerves: the Schwann cell, myelin, axon and the different genes involved in causing neuropathies. Diagnosis is based on data from the clinical history, physical examination and electromyography and their correlation with the type of inheritance in relation to the different genes localized to (a) the Schwann cell: periaxin gene (PRX) encoding L and S periaxin. Stabilisation of the myelin acting as a signal tranducer. NDRG1 down stream regulated gene 1 and 2 acting as transcription factors in embryogenesis. EGR2/Krox 20 has an important function in myelinization. (b) Myelin: P0 membrane protein zero (MPZ) stabilizes the myelin. P1 myelin basic protein (MBP), is analogous to the myelin protein of the central nervous system (CNS) P2 found in the cytoplasm. PMP22 (peripheral myelin protein) also stabilizes the protein. MAG (myelin associated glycoprotein) has antigenic properties. (c). Axon. A foundational mutation (892C Y) in the gene of the lamina (LMNA) of the light neurofilaments (NF L). Mutations in the KIF1Bb gene which encodes the protein kinesin. We also make an aetiological analysis of some classical syndromes, especially the D jerine Sottas syndrome. CONCLUSION: The systematization used, based on clinical and electrophysiological data in relation to the different genes involved in the various anatomical structures constitutes a logical, diagnostic approach which is very useful.

Axons↗

PubMed1998

Coexpression of a constitutively active plasma membrane calcium pump with GFP identifies roles for intracellular calcium in controlling cell sorting during morphogenesis in Dictyostelium.

To examine the potential role of calcium in regulating Dictyostelium development, we reduced free cytosolic and total cell Ca2+ in Dictyostelium cells by expressing a constitutively active form of a human erythrocyte plasma membrane calcium pump. The pump-expressing cells lacked a thapsigargin-mediated increase in cytoplasmic calcium, consistent with a reduced level of total cellular Ca2+. During aggregation, the cells initially formed a large number of aggregation centers, many of which coalesced to form mounds that were smaller than those of wild-type cells, and the cells did not exhibit the normal formation of elongated aggregation streams. The majority of the mounds either arrested at this stage with the formation of small protrusions or formed very aberrant finger-like structures, indicating an essential role for cellular calcium in morphogenesis. We used pump and wild-type cells differentially labeled by expressing different wavelength (green and blue) forms of green fluorescent protein and three-dimensional (3-D) reconstruction of serial fluorescent imaging to visualize the movement of pump and wild-type cells within the aggregate. The results showed that the pump cells exhibited very aberrant cell movement and sorting within the forming mound, suggesting that the reduced cytosolic calcium affects movement required for tip formation. When allowed to form chimeric organisms with wild-type cells, pump cells preferentially localized to two bands, one at the prestalk/prespore boundary and the other in the very posterior of the organism, suggesting that pump cells are unable to properly sort. Expression of the calcium pump had little effect on the induction of prestalk- or prespore-specific genes, whereas extended treatment with EGTA blocked induction of both classes of cell-type-specific genes. Our results suggest a role for intracellular Ca2+ in controlling cell sorting and morphogenesis in Dictyostelium.

Animals↗

PubMedDate not supplied

Intensified process for the purification of an enzyme from inclusion bodies using integrated expanded bed adsorption and refolding.

This work describes the integration of expanded bed adsorption (EBA) and adsorptive protein refolding operations in an intensified process used to recover purified and biologically active proteins from inclusion bodies expressed in E. coli. Delta(5)-3-Ketosteroid isomerase with a C-terminal hexahistidine tag was expressed as inclusion bodies in the cytoplasm of E. coli. Chemical extraction was used to disrupt the host cells and simultaneously solubilize the inclusion bodies, after which EBA utilizing immobilized metal affinity interactions was used to purify the polyhistidine-tagged protein. Adsorptive refolding was then initiated in the column by changing the denaturant concentration in the feed stream from 8 to 0 M urea. Three strategies were tested for performing the refolding step in the EBA column: (i) the denaturant was removed using a step change in feed-buffer composition, (ii) the denaturant was gradually removed using a gradient change in feed-buffer composition, and (iii) the liquid flow direction through the column was reversed and adsorptive refolding performed in the packed bed. Buoyancy-induced mixing disrupted the operation of the expanded bed when adsorptive refolding was performed using either a step change or a rapid gradient change in feed-buffer composition. A shallow gradient reduction in denaturant concentration of the feed stream over 30 min maintained the stability of the expanded bed during adsorptive refolding. In a separate experiment, buoyancy-induced mixing was completely avoided by performing refolding in a settled bed, which achieved comparable yields to refolding in an expanded bed but required a slightly more complex process. A total of 10% of the available KSI-(His(6)) was recovered as biologically active and purified protein using the described purification and refolding process, and the yield was further increased to 19% by performing a second iteration of the on-column refolding operation. This process should be applicable for other polyhistidine tagged proteins and is likely to have the greatest benefit for proteins that tend to aggregate when refolded by dilution.

Adsorption↗