Search results for "proinflammatory cytokine"

showing 10 items of 454 documents

Anti-inflammatory actions of the heme oxygenase-1 pathway.

2003

Heme oxygenase 1 (HO-1) is induced by oxidative or nitrosative stress, cytokines and other mediators produced during inflammatory processes, likely as part of a defence system in cells exposed to stress to provide a negative feedback for cell activation and the production of mediators, which could modulate the inflammatory response. HO-1 activity results in the inhibition of oxidative damage and apoptosis, with significant reductions in inflammatory events including edema, leukocyte adhesion and migration, and production of inflammatory cytokines. HO-1 is induced by nitric oxide (NO) in different biological systems and can control the increased production of this mediator observed in many i…

Chemokinemedicine.medical_treatmentInflammationmedicine.disease_causeProinflammatory cytokineDrug DiscoverymedicineAnimalsHumansPharmacologyInflammationbiologyChemistryAnti-Inflammatory Agents Non-SteroidalMembrane ProteinsCell biologyHeme oxygenaseCytokineImmunologyHeme Oxygenase (Decyclizing)biology.proteinmedicine.symptomSignal transductionCell activationOxidative stressHeme Oxygenase-1Signal TransductionCurrent pharmaceutical design
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Dependence on nuclear factor of activated T-cells (NFAT) levels discriminates conventional T cells from Foxp3 + regulatory T cells

2012

Several lines of evidence suggest nuclear factor of activated T-cells (NFAT) to control regulatory T cells: thymus-derived naturally occurring regulatory T cells (nTreg) depend on calcium signals, the Foxp3 gene harbors several NFAT binding sites, and the Foxp3 (Fork head box P3) protein interacts with NFAT. Therefore, we investigated the impact of NFAT on Foxp3 expression. Indeed, the generation of peripherally induced Treg (iTreg) by TGF-β was highly dependent on NFAT expression because the ability of CD4 + T cells to differentiate into iTreg diminished markedly with the number of NFAT family members missing. It can be concluded that the expression of Foxp3 in TGF-β–induced iTreg depends…

Chromatin ImmunoprecipitationAdoptive cell transferT-LymphocytesImmunoblottingFluorescent Antibody TechniqueLymphocyte ActivationT-Lymphocytes RegulatoryAutoimmune DiseasesProinflammatory cytokineMiceTransforming Growth Factor betaAnimalsHumansHomeodomain ProteinsMultidisciplinaryNFATC Transcription FactorsbiologyFOXP3Forkhead Transcription FactorsNFATTransforming growth factor betaBiological SciencesColitisFlow CytometryNFATC Transcription FactorsAdoptive TransferMolecular biologyCell biologyTransplantationCyclosporinebiology.proteinChromatin immunoprecipitationProceedings of the National Academy of Sciences
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Endoplasmic reticulum‐resident chaperones modulate the inflammatory and angiogenic responses of endothelial cells

2015

SummaryBackground Wound healing depends on a well-balanced regulation of inflammation and angiogenesis. In chronic wounds the healing process is disturbed and inflammation persists. Regulation of wound closure is controlled by transmembrane and extracellular proteins, the folding and maturation of which occur in the endoplasmic reticulum (ER) by ER-resident chaperone machinery. Objectives To study the role of the ER-resident chaperones BiP/Grp78, its cochaperone Mdg1/ERdJ4, and Grp94 in chronic, nonhealing wounds. Methods Immunohistochemical staining of these chaperones in individual human biopsies and investigation of the possible role of BiP and Mdg1 in endothelial cells, focusing on thei…

Chronic woundChemokineAngiogenesisDown-RegulationNeovascularization PhysiologicInflammationDermatologyEndoplasmic ReticulumProinflammatory cytokinemedicineHumansEndoplasmic Reticulum Chaperone BiPCells CulturedHeat-Shock ProteinsInflammationWound HealingMembrane GlycoproteinsbiologyTumor Necrosis Factor-alphaEndoplasmic reticulumEndothelial CellsMembrane ProteinsHSP40 Heat-Shock ProteinsCell biologyChaperone (protein)Chronic Diseasebiology.proteinmedicine.symptomWound healingMolecular ChaperonesBritish Journal of Dermatology
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A variant of Smurf2 protects mice against colitis-associated colon cancer by inducing transforming growth factor β signaling.

2011

Background & Aims Transforming growth factor (TGF)-β signaling, which is down-regulated by the E3 ubiquitin ligase Smad ubiquitin regulating factor 2 (Smurf2), promotes development of cancer. We identified a splice variant of Smurf2 (ΔE2Smurf2) and investigated its role in colon carcinogenesis in mice. Methods Colitis-associated colon cancer was induced in mice by administration of azoxymethane, followed by 3 cycles of oral administration of dextran sodium sulfate. Messenger RNA levels of Smurf2 in colon tumors and control tissue were measured by quantitative polymerase chain reaction; lymphocyte and cytokine levels were measured in tumor and tissue samples. Results Tumor-infiltrating CD4 +…

Colorectal cancermedicine.medical_treatmentLymphocyteUbiquitin-Protein LigasesSMADBiologyProinflammatory cytokineReceptors G-Protein-Coupledchemistry.chemical_compoundMiceTransforming Growth Factor betamedicineAnimalsCells CulturedHepatologyAzoxymethaneGene Expression ProfilingGastroenterologymedicine.diseaseColitisMolecular biologyUbiquitin ligaseMice Inbred C57BLProto-Oncogene Proteins c-kitCytokinemedicine.anatomical_structureHyaluronan ReceptorschemistryColonic Neoplasmsbiology.proteinCancer researchTransforming growth factorSignal TransductionGastroenterology
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Activation of the human immune system via toll-like receptors by the oncolytic parvovirus H-1.

2012

This study aimed to investigate the function of toll-like receptors (TLRs) during oncolytic parvovirus H-1 (H-1PV)-induced human immune responses. First, the role of TLRs in the activation of the NFκB transcription factor was characterized; second, the immunologic effects of H-1PV-induced tumor cell lysates (TCL) on human antitumor immune responses were evaluated. A human ex vivo model was used to study immune responses with dendritic cells (DCs). Human embryonic kidney cells (HEK293) transfected to stably express TLRs were used as potential human DC equivalents to further investigate the role of specific TLRs during immune activation. TLR3 and TLR9 were activated by H-1PV infection, which …

Cytotoxicity ImmunologicH-1 parvovirusCancer ResearchCytoplasmParvovirus H-1chemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent AssayBiologyKidneyProinflammatory cytokineParvoviridae InfectionsImmune systemTumor Cells CulturedHumansMelanomaCells CulturedCell NucleusOncolytic VirotherapyTumor Necrosis Factor-alphaToll-Like ReceptorsNF-kappa BDendritic CellsAcquired immune systemFlow CytometryCell biologyOncolytic virusOncolytic VirusesOncologyImmune SystemImmunologyTLR3CytokinesTumor necrosis factor alphaSignal transductionSignal TransductionInternational journal of cancer
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Impaired Mast Cell-Driven Immune Responses in Mice Lacking the Transcription Factor NFATc2

2009

Abstract The three calcium-dependent factors NFATc1, c2, and c3 are expressed in cells of the immune system and play pivotal roles in modulating cellular activation. With regard to NFATc2, it was reported that NFATc2-deficient mice display increased immune responses in several models for infection and allergy in vivo. This led to the assumption that NFATc2 is involved in the maintenance of immune homeostasis. Using the synthetic TLR7 agonist imiquimod as an adjuvant in epicutaneous peptide immunization, we observed that both the inflammatory reaction and the peptide-specific CTL response are severely impaired in NFATc2-deficient mice. Detailed analyses revealed that early production of proi…

Cytotoxicity ImmunologicImmunologyMice TransgenicInflammationBiologyProinflammatory cytokineMiceImmune systemAdjuvants ImmunologicCell MovementmedicineAnimalsImmunology and AllergyMast CellsLymph nodeInflammationNFATC Transcription FactorsReverse Transcriptase Polymerase Chain ReactionTLR7Flow CytometryMast cellAcquired immune systemCTL*medicine.anatomical_structureLangerhans CellsImmunologyInflammation Mediatorsmedicine.symptomThe Journal of Immunology
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Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14)

2021

Abdominal aortic aneurysm (AAA), is a complex disorder characterized by vascular vessel wall remodeling. LIGHT (TNFSF14) is a proinflammatory cytokine associated with vascular disease. In the present study, the impact of genetic inactivation of Light was investigated in dissecting AAA induced by angiotensin II (AngII) in the Apolipoprotein E-deficient (Apoe−/−) mice. Studies in aortic human (ah) vascular smooth muscle cells (VSMC) to study potential translation to human pathology were also performed. AngII-treated Apoe−/−Light−/− mice displayed increased abdominal aorta maximum diameter and AAA severity compared with Apoe−/− mice. Notably, reduced smooth muscle α-actin+ area and Acta2 and C…

Dissecting Abdominal Aortic Aneurysmmedicine.medical_specialtyVascular smooth musclebiologyApolipoprotein BQH301-705.5ChemistryMedicine (miscellaneous)Angiotensin IIArticleTNFSF14/LIGHTGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineabdominal aortic aneurysmEndocrinologyLymphotoxinInternal medicinecardiovascular systembiology.proteinmedicinevascular smooth muscle cellsGene silencingBiology (General)ACTA2Biomedicines
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Role of Myeloid-Epithelial-Reproductive Tyrosine Kinase and Macrophage Polarization in the Progression of Atherosclerotic Lesions Associated With Non…

2019

Recent lines of evidence highlight the involvement of myeloid-epithelial-reproductive tyrosine kinase (MerTK) in metabolic disease associated with liver damage. MerTK is mainly expressed in anti-inflammatory M2 macrophages where it mediates transcriptional changes including suppression of proinflammatory cytokines and enhancement of inflammatory repressors. MerTK is regulated by metabolic pathways through nuclear sensors including LXRs, PPARs, and RXRs, in response to apoptotic bodies or to other sources of cholesterol. Nonalcoholic fatty liver disease (NAFLD) is one of the most serious public health problems worldwide. It is a clinicopathological syndrome closely related to obesity, insuli…

Drug targeting0301 basic medicineMacrophageMacrophage polarizationInflammationReviewMonocyteProinflammatory cytokine03 medical and health sciencesMerTK0302 clinical medicineFibrosisNonalcoholic fatty liver diseasemedicineNonalcoholic fatty liver diseaseMacrophagePharmacology (medical)InflammationPharmacologybusiness.industrylcsh:RM1-950Lipid metabolismMERTKmedicine.diseasemacrophagesAtherosclerosis; Drug targeting; Inflammation; Macrophages; MerTK; Monocytes; Nonalcoholic fatty liver diseaselcsh:Therapeutics. Pharmacology030104 developmental biologyAtherosclerosi030220 oncology & carcinogenesisCancer researchatherosclerosismedicine.symptommonocytesbusinessFrontiers in Pharmacology
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Endothelin-1 modulates the expression of adhesion molecules on fibroblast-like synovial cells (FLS)

1996

Endothelin-1 is known to possess various biological properties. In the present study we have investigated the effects of Endothelin-1 (Et-1) on the expression of adhesion molecules ICAM-1, VCAM-1 and CD-44 by fibroblast-like synoviocytes. Cultured fibroblast-like synoviocytes were treated with Et-1 in the absence or presence of C1306, a specific endothelin-A-receptor antagonist. Cell surface expression of ICAM-1, VCAM-1 and CD-44 was determined by immunofluorescence studies, Cyto-ELISA and FACS-analysis. ICAM-1, VCAM-1 and CD-44 were constitutively expressed on cultured FLS. After incubation with Et-1 the expression of ICAM-1, VCAM-1 and CD-44 increased. The level of expression of adhesion …

Endothelin Receptor Antagonistsmedicine.medical_specialtymedicine.medical_treatmentImmunologyVascular Cell Adhesion Molecule-1BiologyProinflammatory cytokineRheumatologyDownregulation and upregulationInternal medicinemedicineHumansImmunology and AllergyCells CulturedEndothelin-1Tumor Necrosis Factor-alphaCell adhesion moleculeSynovial MembraneGeneral MedicineAdhesionFibroblastsIntercellular Adhesion Molecule-1Receptor Endothelin AIn vitroCell biologyHyaluronan ReceptorsCytokinemedicine.anatomical_structureEndocrinologyCell cultureSynovial membraneCell Adhesion MoleculesInterleukin-1
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Association of erythrocyte deformability with red blood cell distribution width in metabolic diseases and thalassemia trait.

2016

Abstract Increased red blood distribution width (RDW) in anemia is related to disturbances in the cellular surface/volume ratio, usually accompanied by morphological alterations, while it has been shown in inflammatory diseases that the activity of pro-inflammatory cytokines disturbing erythropoiesis increases RDW. Recently it has been reported that higher RDW is related with decreased erythrocyte deformability, and that it could be related with the association of RDW and increased risk of cardiovascular diseases. In order to analyze the influence of morphological alterations and proinflammatory status on the relationship between RDW and erythrocyte deformability, we analyzed erythrocyte de…

Erythrocyte IndicesMalemedicine.medical_specialtyErythrocytesPhysiologyAnemiaThalassemia030204 cardiovascular system & hematologyBiologyProinflammatory cytokine03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicineErythrocyte DeformabilitymedicineErythrocyte deformabilityHumansMetabolic SyndromeRed blood cell distribution widthHematologymedicine.diseaseEndocrinology030220 oncology & carcinogenesisImmunologyErythrocyte CountErythropoiesisAnisocytosisThalassemiaMetabolic syndromeCardiology and Cardiovascular MedicineClinical hemorheology and microcirculation
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