Search results for "messenger"

showing 10 items of 1493 documents

Antibodies to proteinase 3 mediate expression of vascular cell adhesion molecule-1 (VCAM-1).

1996

SUMMARY VCAM-1 was first identified as an adhesion molecule induced on human endothelial cells (HEC) by inflammatory cytokines such as IL-1, tumour necrosis factor (TNF), and lipopolysaccharide (LPS). The molecule binds to a variety of leucocytes, including B cells, T cells, basophils, eosinophils and monocytes. Vascular expression of VCAM-1 has been associated with a number of disease states, including rheumatoid arthritis and vasculitis. The detection of antineutrophil cytoplasmic antibodies (ANCA), especially to proteinase 3 (PR3), has become important in the diagnosis of Wegener’s granulomatosis (WG) and related vasculitides. Recently we were able to demonstrate a direct effect of anti-…

MyeloblastinT-LymphocytesImmunologyMolecular Sequence DataVascular Cell Adhesion Molecule-1BiologyAntibodiesProinflammatory cytokinechemistry.chemical_compoundAntigenProteinase 3Cell AdhesionImmunology and AllergyHumanscardiovascular diseasesRNA MessengerVCAM-1Cell adhesionCells CulturedBase SequenceCell adhesion moleculeSerine EndopeptidasesOriginal ArticleschemistryImmunologybiology.proteinTumor necrosis factor alphaEndothelium VascularAntibodyClinical and experimental immunology
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Neutrophil extracellular traps mediate transfer of cytoplasmic neutrophil antigens to myeloid dendritic cells toward ANCA induction and associated au…

2012

AbstractAntineutrophil cytoplasmic antibodies (ANCAs) target proteins normally retained within neutrophils, indicating that cell death is involved in the autoimmunity process. Still, ANCA pathogenesis remains obscure. ANCAs activate neutrophils inducing their respiratory burst and a peculiar form of cell death, named NETosis, characterized by formation of neutrophil extracellular traps (NETs), decondensed chromatin threads decorated with cytoplasmic proteins endorsed with antimicrobial activity. NETs have been consistently detected in ANCA-associated small-vessel vasculitis, and this association prompted us to test whether the peculiar structure of NET favors neutrophil proteins uploading i…

MyeloidNeutrophilsApoptosisAutoimmunitymedicine.disease_causeAutoantigensBiochemistryAutoimmunityImmunoenzyme TechniquesMiceCytosolMyeloid CellsSkinMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionANCACell DifferentiationHematologyFlow CytometryAcquired immune systemCell biologyRespiratory burstmedicine.anatomical_structureFemaleANCA; Neutrophil extracellular traps; myeloid dendritic cells; autoimmunity.Programmed cell deathBlotting WesternImmunologyautoimmunity.Anti-Neutrophil Cytoplasmic Antibody-Associated VasculitisEnzyme-Linked Immunosorbent AssayBiologyReal-Time Polymerase Chain ReactionAntibodies Antineutrophil CytoplasmicAntigenmedicineAnimalsHumansRNA Messengercardiovascular diseasesCell ProliferationAnti-neutrophil cytoplasmic antibodyDendritic CellsCell BiologyNeutrophil extracellular trapsmyeloid dendritic cellMice Inbred C57BLImmunologyImmunizationNeutrophil extracellular trap
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CXCR3-ligand-mediated skin inflammation in cutaneous lichenoid graft-versus-host disease.

2007

Background Lichenoid graft-versus-host disease (liGVHD) histologically shares several common features with other lichenoid dermatoses, such as cutaneous lupus erythematosus and lichen planus (LP), which collectively show a junctional infiltrate of cytotoxic lymphocytes with liquefaction of the basal layer ("interface dermatitis"). Because recent studies have shown a role for type I interferon (IFN)–associated inflammation, including lymphocyte recruitment via CXCR3 ligand interaction in cutaneous lupus erythematosus and LP, we hypothesized that similar mechanisms might also be involved in liGVHD. Methods Ten representative lesional skin biopsies taken from patients with different subsets of…

Myxovirus Resistance ProteinsChemokinePathologymedicine.medical_specialtyLichenoid EruptionsReceptors CXCR3CD3T-LymphocytesGraft vs Host DiseaseInflammationDermatitisDermatologyIn situ hybridizationCXCR3LigandsChemokine CXCL9Skin DiseasesGTP-Binding ProteinsMedicineCXCL10HumansLymphocytesRNA MessengerIn Situ Hybridizationbiologybusiness.industryLichen PlanusInterferon-alphaChemokine CXCL10stomatognathic diseasesImmunologyChronic DiseaseInterferon Type Ibiology.proteinCXCL9Immunohistochemistrymedicine.symptomEpidermisbusinessJournal of the American Academy of Dermatology
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Cancer cell–autonomous contribution of type I interferon signaling to the efficacy of chemotherapy

2014

International audience; The immune system is routinely confronted with cell death resulting from the physiological turnover of renewable tissues, as well as from pathological insults of several types. We hypothesize the existence of a mechanism that allows the immune system to discriminate between physiological and pathological instances of cell death, but the factors that determine whether cellular demise is perceived as a neutral, tolerogenic or immunogenic event remain unclear 1. Infectious insults are accompanied by so-called microbe-associated molecular patterns (MAMPs), i.e., viral or bacterial products that activate immune cells through a panel of pattern-recognition receptors (PRRs)…

Myxovirus Resistance ProteinsMessengerReceptor Interferon alpha-betaInbred C57BLchemotherapyInterferon alpha-betaMiceInterferonReceptorsAnthracyclinesNeoplasm MetastasisRIG-IPattern recognition receptorAdaptor ProteinsGeneral MedicineNeoadjuvant Therapy3. Good healthGene Expression Regulation NeoplasticTreatment OutcomeReceptors Pattern RecognitionInterferon Type I[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleImmunocompetencemedicine.drugReceptorSignal TransductionBreast Neoplasms[SDV.CAN]Life Sciences [q-bio]/CancerBiologyPattern RecognitionSettore BIO/09General Biochemistry Genetics and Molecular BiologyParacrine signallingImmune systemmedicineCXCL10AnimalsHumanscancerRNA MessengerAutocrine signallingNeoplastic[SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/ImmunotherapyToll-Like Receptor 3Mice Inbred C57BLVesicular TransportChemokine CXCL10Adaptor Proteins Vesicular TransportGene Expression RegulationDoxorubicinImmunologyTLR3RNAAdaptor Proteins Vesicular Transport; Animals; Anthracyclines; Breast Neoplasms; Chemokine CXCL10; Doxorubicin; Female; Gene Expression Regulation Neoplastic; Humans; Immunocompetence; Interferon Type I; Mice Inbred C57BL; Myxovirus Resistance Proteins; Neoadjuvant Therapy; Neoplasm Metastasis; RNA; RNA Messenger; Receptor Interferon alpha-beta; Receptors Pattern Recognition; Toll-Like Receptor 3; Treatment Outcome; Signal Transduction
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Oxidative stress upregulates the NMDA receptor on cerebrovascular endothelium.

2009

N-methyl-d-aspartate receptor (NMDA-R)-mediated oxidative stress has been implicated in blood-brain barrier (BBB) disruption in a variety of neuropathological diseases. Although some interactions between both phenomena have been elucidated, possible influences of reactive oxygen species (ROS) on the NMDA-R itself have so far been neglected. The objective of this study was to examine how the cerebroendothelial NMDA-R is affected by exposure to oxidative stress and to assess possible influences on BBB integrity. RT-PCR confirmed several NMDA-R subunits (NR1, NR2B-D) expressed in the bEnd3 cell line (murine cerebrovascular endothelial cells). NR1 protein expression after exposure to ROS was ob…

N-MethylaspartateEndotheliumBlotting WesternGlutamic AcidStimulationApoptosismedicine.disease_causeBlood–brain barrierBiochemistryReceptors N-Methyl-D-AspartateImmunoenzyme Techniqueschemistry.chemical_compoundMicePhysiology (medical)medicineAnimalsRNA MessengerCells Culturedchemistry.chemical_classificationReactive oxygen speciesChemistrySuperoxideReverse Transcriptase Polymerase Chain ReactionCell biologyOxidative Stressmedicine.anatomical_structurenervous systemBiochemistryBlood-Brain BarrierCerebrovascular CirculationNMDA receptorEndothelium VascularReactive Oxygen SpeciesPeroxynitriteOxidative stressFree radical biologymedicine
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Loss of Nrf2 in bone marrow-derived macrophages impairs antigen-driven CD8+ T cell function by limiting GSH and Cys availability

2015

NF-E2-related factor 2 (Nrf2), known to protect against reactive oxygen species, has recently been reported to resolve acute inflammatory responses in activated macrophages. Consequently, disruption of Nrf2 promotes a proinflammatory macrophage phenotype. In the current study, we addressed the impact of this macrophage phenotype on CD8(+) T cell activation by using an antigen-driven coculture model consisting of Nrf2(-/-) and Nrf2(+/+) bone marrow-derived macrophages (BMDMΦ) and transgenic OT-1 CD8(+) T cells. OT-1 CD8(+) T cells encode a T cell receptor that specifically recognizes MHC class I-presented ovalbumin OVA(257-264) peptide, thereby causing a downstream T cell activation. Interes…

NF-E2-Related Factor 2OvalbuminAntiporterT cellBlotting WesternReceptors Antigen T-CellApoptosisMice TransgenicCD8-Positive T-LymphocytesBiologyReal-Time Polymerase Chain Reactionenvironment and public healthBiochemistryAntioxidantsImmunoenzyme TechniquesMicechemistry.chemical_compoundBone MarrowPhysiology (medical)MHC class ImedicineAnimalsCytotoxic T cellRNA MessengerCells CulturedCell ProliferationMice KnockoutReverse Transcriptase Polymerase Chain ReactionGCLMMacrophagesHistocompatibility Antigens Class IGlutathionerespiratory systemFlow CytometryGlutathioneMolecular biologyMice Inbred C57BLOxidative Stressmedicine.anatomical_structurechemistrybiology.proteinCystineReactive Oxygen SpeciesIntracellularCD8Signal TransductionFree Radical Biology and Medicine
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dsRNA-functionalized multifunctional gamma-Fe2O3 nanocrystals: a tool for targeting cell surface receptors.

2008

NanoparticleMaghemiteNanotechnologyReceptors Cell Surfaceengineering.materialKidneyLigandsFerric CompoundsCatalysisMagneticsDrug Delivery SystemsCell surface receptorCell Line TumorMoleculeHumansRNA MessengerRNA Double-StrandedFerric CompoundsMolecular StructureChemistryGeneral ChemistryToll-Like Receptor 3RNA silencingNanocrystalBiophysicsengineeringNanoparticlesBiosensorAngewandte Chemie (International ed. in English)
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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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Expression of the proto-oncogene c-myc in human stenotic aortocoronary bypass grafts.

2002

Summary Proliferation and differentiation of vascular smooth muscle cells (VSMC) are central events in vascular pathobiology and play a major role in the development of stenotic and restenotic lesions [ 15, 27 ] . The proto-oncogene c-myc and other early cell cycle-regulating genes have been implicated in the induction of cell proliferation and differentiation under diverse pathophysiological conditions [ 11, 13 ] . In the present study we analyzed c-myc mRNAexpression by indirect nonradioactive in situ hybridization technique (NISH) in human stenotic venous bypass grafts (n = 32) retrieved during re-do operations of coronary artery disease and compared the results with 28 native veins (ven…

NeointimaAdultMalePathologymedicine.medical_specialtyVascular smooth muscleCellIn situ hybridizationBiologyProto-Oncogene MasPathology and Forensic MedicineCoronary artery diseaseProto-Oncogene Proteins c-mycmedicineHumansSaphenous VeinRNA MessengerCoronary Artery BypassIn Situ HybridizationAgedOncogeneGraft Occlusion VascularCell BiologyMiddle Agedmedicine.diseasePathophysiologyBlood Vessel Prosthesismedicine.anatomical_structureVasa vasorumFemalePathology, research and practice
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Caki-1 cells as a model system for the interaction of renally secreted drugs with OCT3.

2008

<i>Background/Aims:</i> Organic cation transporters (OCT) in the proximal tubules (PTs) participate in the renal secretion of several therapeutic agents. The exact role of OCT3 in renal secretion remains undetermined, partially due to the lack of an appropriate in vitro model system. The current work introduces the PT representative cell line, Caki-1, as a model system for studying the involvement of OCT3 in renal secretion. <i>Methods:</i> Caki-1 cells were characterized for OCT3 expression via real-time RT-PCR and immunocytochemical staining techniques. Uptake kinetics of OCT3 in Caki-1 cells was determined using prototypical substrates and inhibitors. Inhibition o…

Nephrologymedicine.medical_specialty1-Methyl-4-phenylpyridiniumOrganic Cation Transport ProteinsPhysiologyCell SurvivalUrinary systemmacromolecular substancesPharmacologyurologic and male genital diseasesCell LineXenobioticsKidney Tubules ProximalPhysiology (medical)Internal medicinemedicineHumansSecretionRNA MessengerKidneyOrganic cation transport proteinsbiologyDose-Response Relationship Drugbusiness.industryOrganic Cation Transporter 1Organic Cation Transporter 2Epithelial CellsGeneral MedicineDrug interactionmedicine.diseaseImmunohistochemistryQuaternary Ammonium CompoundsKineticsEndocrinologymedicine.anatomical_structureNephrologyRenal physiologybiology.proteinbusinessKidney diseaseNephron. Physiology
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