Search results for "Extracellular"

showing 10 items of 1220 documents

Regulation of the effects of CYP2E1-induced oxidative stress by JNK signaling

2014

The generation of excessive amounts of reactive oxygen species (ROS) leads to cellular oxidative stress that underlies a variety of forms of hepatocyte injury and death including that from alcohol. Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). In response to alcohol, hepatocytes have increased levels of the enzyme cytochrome P450 2E1 (CYP2E1) which generates an oxidant stress that promotes the development of alcoholic steatosis and liver injury. These effects are mediated in larg…

Alcoholic liver diseaseClinical BiochemistryReview ArticleMitogen-activated protein kinase kinasemedicine.disease_causeBiochemistryCytochrome P450 2E10302 clinical medicineMolecular Targeted TherapyMitogen-activated protein kinaseslcsh:QH301-705.5c-Jun N-terminal kinasechemistry.chemical_classificationTNF tumor necrosis factorlcsh:R5-9200303 health sciencesCell DeathCYP2E1 cytochrome P450 2E1Cytochrome P-450 CYP2E13. Good healthCell biologyPKD protein kinase DLiverJNK c-Jun N-terminal kinaseSab SH3 homology associated BTK binding protein030211 gastroenterology & hepatologySignal transductionlcsh:Medicine (General)MAP Kinase Signaling SystemAPAP acetaminophenMKK MAPK kinaseBiology03 medical and health sciencesROS reactive oxygen speciesPKC protein kinase CmedicineAnimalsHumansMAPKKK MAPK kinase kinaseProtein kinase ACell damage030304 developmental biologyReactive oxygen speciesMAP kinase kinase kinaseOrganic ChemistryJNK Mitogen-Activated Protein KinasesAlcoholic liver diseasemedicine.diseaseERK1/2 extracellular signal-regulated kinase 1/2Fatty Liverlcsh:Biology (General)chemistryOxidative stressNAFLD nonalcoholic fatty liver diseaseReactive Oxygen SpeciesMAPK mitogen-activated protein kinaseOxidative stressRedox Biology
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Concanavalin A aggregation and toxicity on cell cultures

2009

A number of neurodegenerative diseases are known to involve protein aggregation. Common mechanisms and structural properties of amyloids are thought to be involved in aggregation-related cytotoxicity. In this context we propose an experimental study on Concanavalin A (Con A) aggregation and use it as a model to study the relationship between cell toxicity and aggregation processes. Depending on solution conditions, Con A aggregation has been monitored by static and dynamic light scattering, Thioflavin T emission, and FTIR absorption. The morphology of different aggregate species was verified by means of Atomic Force Microscopy and Confocal Microscopy. During the aggregation pathway the nati…

AmyloidCell SurvivalBiophysicsApoptosisContext (language use)Protein aggregationMicroscopy Atomic ForceFibrilBiochemistryAnalytical Chemistrychemistry.chemical_compoundProtein structureCell Line TumorSpectroscopy Fourier Transform InfraredConcanavalin AExtracellularHumansProtein Structure QuaternaryCytotoxicityMolecular BiologyNeuronsbiologyChemistryBiochemistryConcanavalin Abiology.proteinThioflavinProtein aggregation Amyloids Citotoxicity Oligomers
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Inhibition of Histone Deacetylase Activity in Human Endometrial Stromal Cells Promotes Extracellular Matrix Remodelling and Limits Embryo Invasion

2011

Invasion of the trophoblast into the maternal decidua is regulated by both the trophoectoderm and the endometrial stroma, and entails the action of tissue remodeling enzymes. Trophoblast invasion requires the action of metalloproteinases (MMPs) to degrade extracellular matrix (ECM) proteins and in turn, decidual cells express tissue inhibitors of MMPs (TIMPs). The balance between these promoting and restraining factors is a key event for the successful outcome of pregnancy. Gene expression is post-transcriptionally regulated by histone deacetylases (HDACs) that unpacks condensed chromatin activating gene expression. In this study we analyze the effect of histone acetylation on the expressio…

Anatomy and PhysiologyGene ExpressionHydroxamic AcidsEndometriumEndocrinologyPregnancyMolecular Cell BiologyCells Culturedreproductive and urinary physiologyRegulation of gene expressionMultidisciplinarybiologyQRObstetrics and GynecologyExtracellular MatrixChromatinCell biologyHistonemedicine.anatomical_structureMatrix Metalloproteinase 9embryonic structuresMatrix Metalloproteinase 2MedicineFemaleHistone deacetylase activityResearch Articlemedicine.drugAdultStromal cellScienceDown-RegulationGene Expression Regulation EnzymologicYoung AdultmedicineHumansEmbryo ImplantationBiologyTissue Inhibitor of Metalloproteinase-3Tissue Inhibitor of Metalloproteinase-1Reproductive SystemTrophoblastUrokinase-Type Plasminogen ActivatorMolecular biologyHistone Deacetylase InhibitorsTrichostatin AAcetylationbiology.proteinStromal CellsDevelopmental Biology
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Neutrophil extracellular traps arm DC vaccination against NPM-mutant myeloproliferation

2021

AbstractNeutrophil extracellular traps (NET) are web-like chromatin structures composed by dsDNA and histones, decorated with anti-microbial proteins. Their interaction with dendritic cells (DC) allows DC activation and maturation toward presentation of NET-associated antigens. Differently from other types of cell death that imply protein denaturation, NETosis preserves the proteins localized onto the DNA threads for proper enzymatic activity and conformational status, including immunogenic epitopes. Besides neutrophils, leukemic cells can release extracellular traps displaying leukemia-associated antigens, prototypically mutant nucleophosmin (NPMc+) that upon mutation translocates from nuc…

AntigenChemistryCytoplasmMutantMyeloproliferationCytotoxic T cellNeutrophil extracellular trapsCD8EpitopeCell biology
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The enemy in you: the interdependency of the localisation and antigenicity of proteins

2009

The subcellular localisation of protein components should be important for their antigenicity. This assumption is derived from the concept of MHC restriction, where CD4 and CD8 T lymphocytes can only interact with MHC II and MHC I surface receptors, respectively. If this mechanism applies, however, then intracellular components should have immunogenic effects mediated by MHC II and CD4 T lymphocytes as soon as they enter the extracellular space. Conversely, extracellular components should generate an immune response that is mediated by MHC I and CD8 lymphocytes when they breach the intracellular space and when they exceed a critical concentration. In this study, these hypotheses were invest…

AntigenicitybiologyAntigenMHC class Ibiology.proteinExtracellularCytotoxic T cellchemical and pharmacologic phenomenaT lymphocyteMHC restrictionCD8Cell biologyInternational Journal of Immunological Studies
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Granulysin‐Dependent Killing of Intracellular and ExtracellularMycobacterium tuberculosisby Vγ9/Vδ2 T Lymphocytes

2001

Contribution of Vgamma9/Vdelta2 T lymphocytes to immune protection against Mycobacterium tuberculosis is still a matter of debate. It was reported earlier that Vgamma9/Vdelta2 T lymphocytes kill macrophages harboring live M. tuberculosis through a granule-dependent mechanism that results in killing of intracellular bacilli. This study found that Vgamma9/Vdelta2 T lymphocytes reduce the viability of both extracellular and intracellular M. tuberculosis. Granulysin and perforin, both detected in Vgamma9/Vdelta2 T lymphocytes, play a major role, which indicates that Vgamma9/Vdelta2 T lymphocytes directly contribute to a protective host response against M. tuberculosis infection.

Antigens Differentiation T-LymphocyteCytotoxicity ImmunologicTuberculosisReceptors Antigen T-Cell alpha-betaT-LymphocytesBiologyMicrobiologyMycobacterium tuberculosisExtracellularmedicineHumansTuberculosisImmunology and AllergyMacrophageGranulysinMacrophagesReceptors Antigen T-Cell gamma-deltaMycobacterium tuberculosisT lymphocytemedicine.diseasebiology.organism_classificationInfectious DiseasesPerforinImmunologybiology.proteinIntracellularThe Journal of Infectious Diseases
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Oxidative burst and neutrophil elastase contribute to clearance of Aspergillus fumigatus pneumonia in mice.

2014

Polymorphonuclear neutrophils (PMN) are important for the control of invasive aspergillosis (IA), a major threat to immunocompromised individuals. For clearance of Aspergillus fumigatus infections, PMN employ their potent oxidative and non-oxidative mechanisms. To clarify the relative contribution of these mechanisms, we analyzed p47(phox-/-), gp91(phox-/-) and elastase (ELA) deficient mice (ELANE) after intratracheal infection with A. fumigatus. Infected p47(phox-/-) and gp91(phox-/-) mice died within 4 days and had a significant higher fungal burden in the lungs compared to wild-type controls. Interestingly, the survival of ELANE mice after infection was unimpaired suggesting that ELA is …

Antigens FungalMice 129 StrainNeutrophilsImmunologyAspergillus fumigatusMicrobiologyMiceImmunityIn vivoCell MovementImmunology and AllergyAnimalsHumansLungCells CulturedColony-forming unitInvasive Pulmonary AspergillosisMice KnockoutImmunity CellularMembrane GlycoproteinsbiologyAspergillus fumigatusElastaseNADPH Oxidaseshemic and immune systemsHematologyNeutrophil extracellular trapsbiology.organism_classificationRespiratory burstMice Inbred C57BLOxidative StressNeutrophil elastaseImmunologyNADPH Oxidase 2biology.proteinLeukocyte ElastaseImmunobiology
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Folate-mediated targeting of polymeric conjugates of gemcitabine.

2005

The synthesis of two new macromolecular prodrugs for active tumor targeting was set up. Gemcitabine (2'-deoxy-2',2'-difluorocytidine) was conjugated to alpha,beta-poly(N-2-hydroxyethyl)-DL-aspartamide (PHEA) through succinyl or diglycolyl hydrolysable spacers. The targeting agent folic acid was attached to the macromolecular backbone through the aminocaproic spacer. The two conjugates [PHEA-(5'-succinylgemcitabine)-1'-carboxypentyl-folamide and PHEA-(5'-diglycolyl-gemcitabine)-1'-carboxypentyl-folamide], were purified and extensively characterised by spectroscopic (UV, IR and NMR) and chromatographic analyses to determine the correct chemical structure, the purity degree and the reaction yi…

Antimetabolites AntineoplasticTime FactorsStereochemistryCell SurvivalpolyaspartamideChemical structurePharmaceutical ScienceReceptors Cell SurfaceConjugated systemDeoxycytidineDrug Delivery SystemsFolic AcidCell Line Tumorfolate-mediated targetingExtracellularHumansProdrugsIncubationPolyhydroxyethyl MethacrylateDrug CarriersDose-Response Relationship DrugChemistrypolymeric conjugateFolate Receptors GPI-AnchoredSuccinatesHydrogen-Ion ConcentrationGemcitabineIn vitroBiochemistryCell cultureCarrier ProteinsMacromoleculeConjugateInternational journal of pharmaceutics
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Antioxidant Pathways in Alzheimers Disease: Possibilities of Intervention

2011

Alzheimer's disease (AD) is closely related to the occurrence of oxidative stress. It was claimed that all pathophysiological mechanisms involved in the onset and progression of AD are related to oxidative stress. Thus, it is important to evaluate if there is oxidative stress as well as the mechanism by which this happens in AD patients as well as in animal models of AD. Extracellular plaques of amyloid b peptides (Aβ), a hallmark of the disease, have been postulated to be more protective than damaging in terms of oxidative stress because they may be chemical sinks in which heavy metals are placed. More than a decade ago we reasoned that damage due to Ab might be caused not by extracellular…

AntioxidantAmyloidmedicine.medical_treatmentRespiratory chainNerve Tissue ProteinsBiologyPharmacologymedicine.disease_causeAntioxidantsAlzheimer DiseaseDrug DiscoverymedicineExtracellularAnimalsHumansMolecular Targeted TherapyPharmacologychemistry.chemical_classificationReactive oxygen speciesEstradiolVitamin Emedicine.diseaseUp-RegulationOxidative StressNeuroprotective AgentschemistryDietary SupplementsImmunologyAlzheimer's diseaseReactive Oxygen SpeciesOxidative stressCurrent Pharmaceutical Design
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Mechanism of vascular relaxation by thaligrisine

2000

Abstract In the present study we examine the mechanism by which thaligrisine, a bisbenzyltetrahydroisoquinoline alkaloid, inhibits the contractile response of vascular smooth muscle. The work includes functional studies on rat isolated aorta and tail artery precontracted with noradrenaline or KCl. In other experiments rat aorta was precontracted by caffeine in the presence or absence of extracellular Ca 2 +. In order to assess whether thaligrisine interacts directly with calcium channel binding sites or with α-adrenoceptors we examined the effect of the alkaloid on [ 3 H]-(+)- cis diltiazem, [ 3 H]-nitrendipine and [ 3 H]-prazosin binding to cerebral cortical membranes. The functional studi…

AortaVascular smooth muscleStereochemistrychemistry.chemical_elementGeneral MedicineCalciumGeneral Biochemistry Genetics and Molecular BiologyTetrandrinechemistry.chemical_compoundchemistrymedicine.arteryExtracellularBiophysicsmedicineChannel blockerCalcium Channel BindingGeneral Pharmacology Toxicology and PharmaceuticsBinding siteLife Sciences
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