Search results for "Lysosome"

showing 10 items of 125 documents

Lysosomal changes related to exercise injuries and training-induced protection in mouse skeletal muscle

1984

Three experiments were designed to study the lysosomal changes associated with the development and maintenance of the endurance training induced resistance against exercise injuries in mouse skeletal muscles. The activities of arylsulphatase, cathepsin C, cathepsin D, and beta-glucuronidase were assayed from the red part of mouse quadriceps femoris muscle 4 days after prolonged strenuous running of 4-9 h duration. Exercise injuries were characterized by necrotic fibers and focal inflammation. Strenuous running of untrained mice induced necrotic lesions and a 4-5 fold increase in the activities of lysosomal enzymes. This lysosomal response was considerably reduced already by daily training b…

Malemedicine.medical_specialtyTime FactorsNecrosisHydrolasesPhysiologyPhysical ExertionCathepsin DCitrate (si)-SynthaseCathepsin CMiceNecrosisPhysical medicine and rehabilitationEndurance trainingInternal medicinemedicineAnimalsExertionArylsulfatasesGlucuronidasebusiness.industryMusclesSkeletal muscleCathepsinsQuadriceps femoris muscleEndocrinologymedicine.anatomical_structuremedicine.symptomLysosomesbusinesshuman activitiesMuscle ContractionMuscle contractionActa Physiologica Scandinavica
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Phase coexistence in a triolein-phosphatidylcholine system. Implications for lysosomal membrane properties.

2010

The effects of tri- and monoglycerides on phospholipid (POPC) membranes were studied using spectroscopical methods. Triolein was found to form two types of POPC-rich membranes, both with POPC or as a three-component system with monopalmitin. These two membrane types were determined as co-existing phases based on their spontaneous and stable separation and named heavy and light phase according to their sedimentation behaviour. Marked differences were seen in the physical properties of these phases, even though only minor compositional variation was detected. The light, less polar phase was found to be less ordered and more fluid and seemed to allow significantly lower amount of water penetra…

Membrane FluidityLipid BilayersPhospholipidCalorimetryBiochemistryPhase TransitionGlycerideschemistry.chemical_compoundPhosphatidylcholineMembrane fluidityTransition TemperatureTrioleinMolecular BiologyPOPCChromatographyCalorimetry Differential ScanningOrganic ChemistryElectron Spin Resonance SpectroscopyWaterCell BiologyPenetration (firestop)MembranechemistryBiophysicsPhosphatidylcholineslipids (amino acids peptides and proteins)LysosomesTrioleinChemistry and physics of lipids
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Splice donor site mutation in the lysosomal neuraminidase gene causing exon skipping and complete loss of enzyme activity in a sialidosis patient.

2001

Sialidosis is a lysosomal storage disease caused by the deficiency of K K-N-acetylneuraminidase (NEU1; sialidase), the key enzyme for the intralysosomal catabolism of sialylated glycoconjugates. We have identified a homozygous transversion in the last intron (IVSE +1 Gs C) in neu1 of a sialidosis patient. Sequencing of the truncated cDNA revealed an alternatively spliced neu1 transcript which lacks the complete sequence of exon 5. Skipping of exon 5 leads to a frameshift and results in a premature termination codon. This is the first description of an intronic point mutation causing a complete deficiency of the lysosomal neuraminidase activity. fl 2001 Federation of Euro- pean Biochemical S…

Molecular Sequence DataBiophysicsNeuraminidaseBiochemistryFrameshift mutationNEU1ExonLysosomal neuraminidaseStructural BiologyMucolipidosesGeneticsLysosomal storage diseasemedicineHumansSialidosisAmino Acid SequenceMolecular BiologyGeneticsSialidosisSplice site mutationbiologySequence Homology Amino AcidReverse Transcriptase Polymerase Chain ReactionDonor splice siteCell BiologyExonsFibroblastsmedicine.diseaseMolecular biologyExon skippingMutationbiology.proteinRNA Splice SitesLysosomesNeuraminidaseExon skippingGene DeletionFEBS letters
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Endocytosis in skeletal muscle fibers.

1999

Defining the organization of endocytic pathway in multinucleated skeletal myofibers is crucial to understand the routing of membrane proteins, such as receptors and glucose transporters, through this system. Here we analyzed the organization of the endocytic trafficking pathways in isolated rat myofibers. We found that sarcolemmal-coated pits and transferrin receptors were concentrated in the I band areas. Fluid phase markers were taken up into vesicles in the same areas along the whole length of the fibers and were then delivered into structures around and between the nuclei. These markers also accumulated beneath the neuromuscular and myotendinous junctions. The recycling compartment, lab…

Monosaccharide Transport ProteinsEndosomeEndocytic cycleMuscle Fibers SkeletalFluorescent Antibody TechniqueGene ExpressionMuscle ProteinsTransferrin receptorEndosomesBiologyEndocytosisMicrotubulesSarcolemmaMicrotubuleReceptors TransferrinMyocyteAnimalsMuscle SkeletalCells Culturedchemistry.chemical_classificationGlucose Transporter Type 4Cell MembraneCoated Pits Cell-MembraneCell BiologyEndocytosisCell biologyCell CompartmentationRatsMicroscopy ElectronMembrane proteinchemistryTransferrinLysosomesExperimental cell research
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Influence of anti-inflammatory flavonoids on degranulation and arachidonic acid release in rat neutrophils.

1994

We assessed the effects of 24 flavonoid derivatives, reported as anti-inflammatory, on lysosomal enzyme secretion and arachidonic acid release in rat neutrophils. Amentoflavone, quercetagetin- 7-O -glucoside, apigenin, fisetin, kaem pferol, luteolin and quercetin were the most potent inhibitors of β-glucuronidase and lysozyme release. The first com pound was also able to inhibit basal release. These flavonoids besides chrysin and to a reduced extent, naringenin, significantly inhibited arachidonic acid release from membranes. A correlation between degranulation and arachidonic acid release was found for this series of compounds. Structureactivity relationships and implications for the anti-…

NaringeninNeutrophilsAmentoflavoneBiologyGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundStructure-Activity RelationshipAnimalsheterocyclic compoundsChrysinGlucuronidaseFlavonoidsArachidonic AcidMolecular StructureAnti-Inflammatory Agents Non-Steroidalfood and beveragesRatsN-Formylmethionine Leucyl-PhenylalaninechemistryBiochemistryApigeninRegression AnalysisArachidonic acidMuramidaseKaempferolLysosomesLuteolinFisetinZeitschrift fur Naturforschung. C, Journal of biosciences
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Influence of cadmium on the morphology and functionality of haemocytes in the compound ascidian Botryllus schlosseri

2013

In order to get insights into the effects of cadmium (Cd) on cell morphology and functions, we exposed haemocytes of the colonial ascidian Botryllus schlosseri to sub-lethal concentrations of CdCl(2). Results indicate that Cd hampers haemocyte spreading and phagocytosis in a dose-dependent way, through the alteration of the actin cytoskeleton. In addition, the metal decreases the stability of the internal membranes, as revealed by the Neutral Red assay. The fraction of cells showing positivity for the lysosomal enzyme acid phosphatase is also reduced in the presence of Cd, whereas the number of cells responsive to the Annexin-V assay and showing chromatin condensation increases, suggesting …

Neutral redHemocytesAscidiansPhysiologyCell SurvivalHealth Toxicology and MutagenesisPhagocytosisApoptosisBotryllus schlosseriToxicologyCell morphologyBiochemistrychemistry.chemical_compoundPhagocytosisSuperoxidesCell AdhesionAnimalsUrochordataBotryllus sp.; Ascidians; Haemocytes; Toxicity; CadmiumHaemocytesbiologyCell DeathToxicitySuperoxideCell MembraneAcid phosphataseCell BiologyGeneral MedicineAnatomyActin cytoskeletonbiology.organism_classificationChromatinPhosphoric Monoester HydrolasesCell biologyActin CytoskeletonOxidative StresschemistryBotryllus spApoptosisbiology.proteinMetallothioneinLysosomesOxidation-ReductionCadmium
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Freeze-fracture features of epithelioid cells, multinucleated giant cells, and phagocytic macrophages

1987

The freeze-fracture morphology of epithelioid cells, multinucleated giant cells (Langhans' type), and phagocytic macrophages was investigated. The intensely folded and interdigitating surface membranes of epithelioid cells and multinucleated giant cells displayed no specialized areas of cell contact. The size of the intramembranous particles (IMP) and the fact that the area density of IMPs was higher in the cytoplasmic (P) faces than in the external (E) faces of the cell membranes agreed with observations in other eukaryotic cells. The area densities of the IMPs suggest lower transport rates of molecules across the cell membranes of granuloma cells than of certain epithelial cells. Small pi…

Nuclear EnvelopeLanghans giant cellBiologyEpitheliumCell membranemedicineAnimalsFreeze FracturingCell NucleusPhagocytesGranulomaNucleoplasmMacrophagesCell MembraneGranule (cell biology)Membrane ProteinsIntracellular MembranesRatsCell biologyCell nucleusmedicine.anatomical_structureGiant cellCytoplasmNephritis InterstitialLysosomesEpithelioid cellVirchows Archiv B Cell Pathology Including Molecular Pathology
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Role of Recycling Endosomes and Lysosomes in Dynein-Dependent Entry of Canine Parvovirus

2002

ABSTRACT Canine parvovirus (CPV) is a nonenveloped virus with a 5-kb single-stranded DNA genome. Lysosomotropic agents and low temperature are known to prevent CPV infection, indicating that the virus enters its host cells by endocytosis and requires an acidic intracellular compartment for penetration into the cytoplasm. After escape from the endocytotic vesicles, CPV is transported to the nucleus for replication. In the present study the intracellular entry pathway of the canine parvovirus in NLFK (Nordisk Laboratory feline kidney) cells was studied. After clustering in clathrin-coated pits and being taken up in coated vesicles, CPV colocalized with coendocytosed transferrin in endosomes r…

Parvovirus CanineEndosomeanimal diseasesvirusesImmunologyDyneinCoated vesicleEndosomesBiologyEndocytosisMicrobiologyMicrotubulesCell LineDogsMicrotubuleVirologyAnimalsMicroscopy ImmunoelectronIn Situ Hybridization FluorescenceMicroscopy ConfocalVesicleEndoplasmic reticulumDyneinsEndocytosisCell biologyVirus-Cell InteractionsCytoplasmInsect ScienceLysosomes
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Intraepidermal morphologic manifestations in lysosomal diseases.

1989

This paper reports the ultrastructural findings for the epidermis of biopsied skin specimens in numerous lysosomal diseases, which can be grouped as follows: a) presence of vacuolar lysosomal residual bodies in mucopolysaccharidoses I, II and III, Salla disease, GM 2 -gangliosidoses and infantile type II glycogenosis; b) avacuolar lysosomal residual bodies in Niemann-Pick disease type C, mucolipidosis IV, Farber disease, Fabry disease, and late infantile and juvenile neuronal ceroid-lipofuscinoses; c) absence of lysosomal residual bodies in GM 2 -gangliosidoses, metachromatic leukodystrophy, Gaucher disease and sialidosis type III Whenever possible, a biopsy of the skin for morphological di…

Pathologymedicine.medical_specialtyBiologyGangliosidosesDevelopmental NeuroscienceLysosomeBiopsymedicineHumansSialidosisSkinInclusion BodiesFarber diseasemedicine.diagnostic_testGeneral Medicinemedicine.diseaseFabry diseaseMetachromatic leukodystrophyMicroscopy Electronmedicine.anatomical_structureSalla diseasePediatrics Perinatology and Child HealthImmunologyNeurology (clinical)LysosomesMetabolism Inborn ErrorsBraindevelopment
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