Search results for "tumor necrosis factor-alpha"

showing 10 items of 504 documents

Induction of collagenase-3 (MMP-13) expression in human skin fibroblasts by three-dimensional collagen is mediated by p38 mitogen-activated protein k…

1999

Collagenase-3 (matrix metalloproteinase-13, MMP-13) is a recently identified human MMP with an exceptionally wide substrate specificity and restricted tissue-specific expression. Here we show that MMP-13 expression is induced in normal human skin fibroblasts cultured within three-dimensional collagen gel resulting in production and proteolytic activation of MMP-13. Induction of MMP-13 mRNAs by collagen gel was potently inhibited by blocking antibodies against alpha1 and alpha2 integrin subunits and augmented by activating antibody against beta1 integrin subunit, indicating that both alpha1 beta1 and alpha2 beta1 integrins mediate the MMP-13-inducing cellular signal generated by three-dimens…

MAPK/ERK pathwayIntegrinsReceptors CollagenSB 203580IntegrinDown-RegulationBiologyBiochemistryp38 Mitogen-Activated Protein KinasesCollagen receptorIntegrin alpha1beta1chemistry.chemical_compoundTransforming Growth Factor betaMatrix Metalloproteinase 13medicineHumansCollagenasesProtein kinase AMolecular BiologyDNA PrimersSkinBase SequenceKinaseTumor Necrosis Factor-alphaCell BiologyFibroblastsProtein-Tyrosine KinasesMolecular biologyEnzyme ActivationchemistryCalcium-Calmodulin-Dependent Protein KinasesCollagenasebiology.proteinCollagenMitogen-Activated Protein KinasesTyrosine kinasemedicine.drugInterleukin-1The Journal of biological chemistry
researchProduct

The stimulation of arginine transport by TNFα in human endothelial cells depends on NF-κB activation

2004

In human saphenous vein endothelial cells (HSVECs), tumor necrosis factor-alpha (TNFalpha) and bacterial lipopolysaccharide (LPS), but neither interferon gamma (IFNgamma) nor interleukin 1beta (IL-1beta), stimulate arginine transport. The effects of TNFalpha and LPS are due solely to the enhancement of system y+ activity, whereas system y+L is substantially unaffected. TNFalpha causes an increased expression of SLC7A2/CAT-2B gene while SLC7A1/CAT-1 expression is not altered by the cytokine. The suppression of PKC-dependent transduction pathways, obtained with the inhibitor chelerytrhine, the inhibitor peptide of PKCzeta isoform, or chronic exposure to phorbol esters, does not prevent TNFalp…

MAPK/ERK pathwayLipopolysaccharidesmedicine.medical_specialtyUmbilical VeinsTime FactorsCAT transporterArginineTranscription Geneticp38 mitogen-activated protein kinasesmedicine.medical_treatmentBiophysicsPharmacologyBiologyArgininePolymerase Chain Reactionp38 Mitogen-Activated Protein KinasesBiochemistryInterferon-gammaInternal medicineCationsmedicineTNFαHumansInterferon gammaRNA MessengerCationic Amino Acid Transporter 2Cells CulturedProtein Kinase CArginine transportReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaNF-kappa BBiological TransportCell BiologyCytokineEndocrinologySLC7 geneAmino Acid Transport Systems BasicCytokinesTumor necrosis factor alphaEndothelium VascularSignal transductionMitogen-Activated Protein KinasesPeptidesmedicine.drugInterleukin-1Signal TransductionNFκBBiochimica et Biophysica Acta (BBA) - Biomembranes
researchProduct

Effect of simultaneous inhibition of TNF-α production and xanthine oxidase in experimental acute pancreatitis: The role of mitogen activated protein …

2004

Javier Pereda et al.

MAPK/ERK pathwayMalemedicine.medical_specialtyXanthine OxidaseOxypurinolPharmacologychemistry.chemical_compoundInternal medicineMedicineAnimalsEnzyme InhibitorsPentoxifyllinePhosphorylationRats WistarXanthine oxidaseProtein kinase ALungPancreasPeroxidasebiologybusiness.industryKinasePancreatitis Acute NecrotizingTumor Necrosis Factor-alphaAscitesOriginal Articlesmedicine.diseaseRatsEnzyme ActivationOxidative StressEndocrinologychemistryMitogen-activated protein kinasebiology.proteinAcute pancreatitisPancreatitisSurgeryTumor necrosis factor alphaInflammation MediatorsMitogen-Activated Protein Kinasesbusiness
researchProduct

Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
researchProduct

Choice of second-line disease-modifying antirheumatic drugs after failure of methotrexate therapy for rheumatoid arthritis: A decision tree for clini…

2009

Objective To survey rheumatologists' preferences for the choice of a second-line disease-modifying antirheumatic drug (DMARD) after inadequate response with methotrexate (MTX) therapy in rheumatoid arthritis (RA). Methods Thirty-six rheumatologists stated their preferences for RA treatment after inadequate response with MTX therapy (optimal dose at least 6 months). From the initial scenario, we derived 54 vignettes varying by rheumatoid factor or anti–cyclic citrullinated peptide antibody presence, swollen joint count, Disease Activity Score in 28 joints, and structural damage. Respondents stated their preference among 5 therapeutic options: MTX continuation, switch to another conventional …

MESH: Antirheumatic AgentsMESH: Decision TreesMESH: Treatment FailureArthritisMESH: Antibodies Anti-IdiotypicMESH: Logistic ModelsLogistic regressionSeverity of Illness IndexArthritis Rheumatoid0302 clinical medicineimmune system diseasesImmunology and AllergyMESH: Data CollectionPharmacology (medical)Treatment Failure030212 general & internal medicinePractice Patterns Physicians'skin and connective tissue diseasesMESH: Arthritis RheumatoidData CollectionAntibodies Anti-Idiotypic3. Good healthMESH: Interleukin 1 Receptor Antagonist ProteinMESH: Methotrexate[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemAntirheumatic AgentsRheumatoid arthritismedicine.drugmusculoskeletal diseasesmedicine.medical_specialtyMESH: Rheumatoid FactorImmunologyPeptides Cyclic03 medical and health sciencesRheumatologyRheumatoid FactorMESH: Severity of Illness IndexInternal medicineSeverity of illnessmedicineHumansRheumatoid factorMESH: Physician's Practice PatternsMESH: Peptides Cyclic030203 arthritis & rheumatologyAnakinraMESH: HumansTumor Necrosis Factor-alphabusiness.industryDecision Treesmedicine.diseaseRheumatologyInterleukin 1 Receptor Antagonist ProteinLogistic ModelsMethotrexateMESH: Tumor Necrosis Factor-alphaPhysical therapyMethotrexatebusinessArthritis & Rheumatism
researchProduct

Cancer in Elderly Onset Inflammatory Bowel Disease: A Population-Based Study.

2016

IF 10.383; International audience; OBJECTIVES: Cancer may be a complication of inflammatory bowel disease (IBD) or its treatment. In elderly onset IBD patients the risk of malignancy is of particular concern. We studied this risk in a population-based cohort of elderly onset IBD patients.METHODS: In a French population-based cohort, we identified 844 patients aged >60 years at IBD diagnosis from 1988 to 2006, including 370 Crohn's disease (CD) and 474 ulcerative colitis (UC). We compared incidence of cancer among IBD patients with that observed in the French Network of population-based Cancer Registries (FRANCIM). Confidence interval (CI) was estimated assuming a Poisson-specific law for ra…

MESH: CarcinomaMaleNonmelanoma Skin-CancerInflammatory bowel disease0302 clinical medicineAdrenal Cortex HormonesAzathioprineMESH: IncidenceAge of OnsetAged 80 and overeducation.field_of_studyMESH: Middle AgedRheumatoid-ArthritisIncidenceGastroenterologyMESH: Follow-Up StudiesMESH: Anti-Inflammatory Agents Non-Steroidal3. Good health030220 oncology & carcinogenesisCohort030211 gastroenterology & hepatology[ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: Immunosuppressive Agentsmedicine.medical_specialtyMESH: Age of OnsetMESH: Colitis Ulcerativedigestive systemMESH: Adrenal Cortex Hormones03 medical and health sciencesIntestinal NeoplasmsHumansCrohns-DiseaseeducationMESH: Intestinal NeoplasmsMESH: Protective FactorsMESH: AzathioprineAgedRetrospective StudiesMESH: HumansMESH: Crohn DiseaseTumor Necrosis Factor-alphaMESH: Retrospective Studiesmedicine.diseaseMESH: Inflammatory Bowel DiseasesInflammatory Bowel Diseasesdigestive system diseasesLymphoproliferative DisordersMethotrexateMESH: Tumor Necrosis Factor-alphaColitis UlcerativeComplicationMESH: FemaleProspective Observational CohortTime FactorsMESH: RegistriesMESH: Proportional Hazards ModelsMaintenance TherapyMESH: Aged 80 and overMESH: Lymphoproliferative DisordersCrohn DiseaseMESH: Risk FactorsRisk FactorsNeoplasmsMESH: NeoplasmsRegistriesUlcerative-ColitisMesalamineMESH: AgedIncidence (epidemiology)Anti-Inflammatory Agents Non-SteroidalMetaanalysisMiddle AgedhumanitiesMESH: MethotrexateFemaleFranceFrench PopulationColorectal NeoplasmsImmunosuppressive AgentsMESH: Myeloproliferative DisordersPopulationColorectal-CancerIncreased RiskInternal medicinemedicineProportional Hazards ModelsMyeloproliferative DisordersHepatologybusiness.industryMESH: Time FactorsCarcinomaCancerRetrospective cohort study[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: MesalamineProtective FactorsMESH: MaleMESH: FranceAge of onsetbusinessMESH: Colorectal NeoplasmsFollow-Up StudiesThe American journal of gastroenterology
researchProduct

Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

2008

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no signifi…

MESH: InflammationGlycosylphosphatidylinositolsNeutrophilsmedicine.medical_treatmentInterleukin-1betasourisMESH: NeutrophilsMESH: VirulenceMESH: Mice KnockoutMiceMESH: Interleukin-1betaNull cellMESH: AnimalsCandida albicansPeritoneal CavityCells CulturedMice Knockout0303 health sciencesToll-like receptorbiologyVirulenceMESH: Toll-Like Receptor 2MESH: Peritoneal CavityMESH: Toll-Like Receptor 4MESH: GlycosylphosphatidylinositolsInfectious DiseasesCytokineMESH: Survival AnalysisTumor necrosis factor alphaMESH: Fungal Proteinsprotéine de la paroi cellulaireMESH: Macrophages PeritonealMESH: Cells CulturedVirulence FactorsImmunologyMicrobiologyMicrobiologyProinflammatory cytokineFungal Proteins03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsMESH: Mice030304 developmental biologyMESH: Virulence FactorsInflammation030306 microbiologyInterleukin-6Tumor Necrosis Factor-alphaMESH: Candida albicans[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologybiology.organism_classificationSurvival AnalysispathogénicitéMESH: Interleukin-6Toll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4TLR2GlycosylphosphatidylinositolMESH: Gene DeletionMESH: Tumor Necrosis Factor-alphaTLR4Macrophages Peritonealcandida albicansimmunitéGene Deletion
researchProduct

Granulocyte-macrophage colony-stimulating factor induces cytokine secretion by human polymorphonuclear leukocytes.

1989

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is known as an inducer of proliferation and functional activation of myeloid cells. This study was carried out to characterize the effects of GM-CSF on polymorphonuclear leukocytes (PMN) more extensively. Using Northern blot analysis, we show that PMN are able to accumulate mRNAs for different cytokines, including tumor necrosis factor-alpha (TNF-alpha); G-CSF, and M-CSF, all of which are involved in inflammation and hematopoiesis. Biological assays and immunoassays demonstrate that PMN translate these mRNAs, except TNF-alpha, into secretory proteins. However, the expression of these cytokines is dependent on stimulation by exogenous…

Macrophage colony-stimulating factorNeutrophilsT cellInflammationBiologyBiological FactorsMiceColony-Stimulating FactorsGranulocyte Colony-Stimulating FactormedicineAnimalsHumansRNA MessengerGrowth SubstancesTumor Necrosis Factor-alphaMacrophage Colony-Stimulating FactorLymphokineGranulocyte-Macrophage Colony-Stimulating FactorGeneral MedicineColony-stimulating factorRecombinant ProteinsRetractionCell biologymedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorImmunologyCytokinesTumor necrosis factor alphaCytokine secretionmedicine.symptomResearch Articlemedicine.drugJournal of Clinical Investigation
researchProduct

Tumor necrosis factor (TNF)-alpha but not TNF-beta induces secretion of colony stimulating factor for macrophages (CSF-1) by human monocytes

1987

Abstract Tumor necrosis factor (TNF)-alpha has been identified as a major inducer of colony stimulating factor (CSF)-secretion by human vascular endothelial cells and fibroblasts. In the present study we assessed the capacity of TNFs to induce release of CSF-1 from highly purified peripheral blood monocyte preparations. Whereas monocytes do not accumulate CSF-1 messenger (m)RNA constitutively and consequently do not produce CSF-1 protein, CSF-1 mRNA and protein secretion became detectable, when monocytes were cultured in the presence of TNF-alpha, that was synergistically enhanced by interferon-gamma (IFN-gamma). However, under identical experimental conditions TNF-beta failed to induce mon…

Macrophage colony-stimulating factormedicine.medical_specialtyT-LymphocytesImmunologyIn Vitro TechniquesBiologyBiochemistryMonocytesColony-Forming Units AssayColony-Stimulating FactorsInternal medicinemedicineHumansSecretionLeukapheresisMessenger RNATumor Necrosis Factor-alphaMonocyteCell BiologyHematologyMacrophage ActivationColony-stimulating factorMolecular biologyHaematopoiesisEndocrinologySecretory proteinmedicine.anatomical_structureTumor necrosis factor alphaBlood
researchProduct

Allopurinol Protective Effect of Renal Ischemia by Downregulating TNF-α, IL-1β, and IL-6 Response

2016

Allopurinol is a well-known antioxidant that protects tissue against ischemia and reperfusion injury, blocking purine catabolism, and possibly reducing TNF-α and other cytokines. It also plays a significant role in reducing the inflammatory processes by inhibiting chemotaxis and other inflammatory mediators. The objective of this study was to define the role of allopurinol regarding kidney ischemic injury particularly as to its effect on inflammatory molecules such as TNF-α, IL-1β, and IL-6 response. One hundred and twenty five rats were subjected to warm renal ischemia. Five more animals were included as sham. Animal survival and plasma levels of lipid peroxidation, myeloperoxidase, lactat…

Male0301 basic medicineAllopurinolDrug Evaluation PreclinicalIschemiaAllopurinolPharmacologyKidneyGout SuppressantsLipid peroxidation03 medical and health scienceschemistry.chemical_compound0302 clinical medicineLactate dehydrogenaseAnimalsMedicineRats WistarKidneybiologyRenal ischemiaInterleukin-6Tumor Necrosis Factor-alphabusiness.industryInterleukin-18Acute Kidney Injurymedicine.disease030104 developmental biologymedicine.anatomical_structurechemistryReperfusion Injury030220 oncology & carcinogenesisMyeloperoxidaseImmunologybiology.proteinSurgerybusinessReperfusion injurymedicine.drugJournal of Investigative Surgery
researchProduct