Search results for "Intercellular adhesion molecule-1"

showing 6 items of 106 documents

IgG anti-endothelial cell antibodies (AECA) in type I diabetes mellitus; induction of adhesion molecule expression in cultured endothelial cells

1998

SUMMARYAECA were detected in 25 of 71 patients with type 1 diabetes mellitus and in two of 33 healthy subjects. Patients with diabetes of < 1 year duration and those with long-standing disease had the highest levels of these antibodies. Inhibition studies suggest that at least part of the AECA reactivity is due to cross-reactive anti-ssDNA antibodies. AECA-positive sera were able to increase intercellular adhesion molecule-1 (ICAM-1) and E-selectin on human umbilical vein endothelial cells (HUVEC). Increased binding of polymorphonuclear (PMN) cells was also found to accompany raised E-selectin expression. Soluble ICAM-1 and E-selectin were also found to be increased in the sera of AE…

medicine.medical_specialtyAdolescentNeutrophilsImmunologyIntercellular Adhesion Molecule-1GranulocyteUmbilical veinInternal medicineE-selectinCell AdhesionmedicineHumansImmunology and AllergyChildCells CulturedAutoantibodiesType 1 diabetesbiologybusiness.industryCell adhesion moleculeIntercellular Adhesion Molecule-1medicine.diseaseEndothelial stem cellDiabetes Mellitus Type 1medicine.anatomical_structureEndocrinologyChild PreschoolImmunoglobulin GImmunologybiology.proteinOriginal ArticleEndothelium VascularAntibodyE-SelectinbusinessClinical and Experimental Immunology
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Retinoid X receptor agonists impair arterial mononuclear cell recruitment through peroxisome proliferator-activated receptor-γ activation.

2012

Abstract Mononuclear cell migration into the vascular subendothelium constitutes an early event of the atherogenic process. Because the effect of retinoid X receptor (RXR)α on arterial mononuclear leukocyte recruitment is poorly understood, this study investigated whether RXR agonists can affect this response and the underlying mechanisms involved. Decreased RXRα expression was detected after 4 h stimulation of human umbilical arterial endothelial cells with TNF-α. Interestingly, under physiological flow conditions, TNF-α–induced endothelial adhesion of human mononuclear cells was concentration-dependently inhibited by preincubation of the human umbilical arterial endothelial cells with RXR…

medicine.medical_specialtyEndotheliumTetrahydronaphthalenesImmunologyPeroxisome proliferator-activated receptorDown-RegulationVascular Cell Adhesion Molecule-1Cell CommunicationRetinoid X receptorBiologyPeripheral blood mononuclear cellUmbilical ArteriesCell LineInternal medicinemedicineImmunology and AllergyHumansReceptorMuscle SkeletalBexarotenechemistry.chemical_classificationRetinoid X Receptor alphaTumor Necrosis Factor-alphaMicrocirculationIntercellular Adhesion Molecule-1Cell biologyPPAR gammaEndocrinologymedicine.anatomical_structureNuclear receptorchemistryBexaroteneCell Migration InhibitionLeukocytes MononuclearEndothelium VascularMononuclear cell migrationmedicine.drugJournal of immunology (Baltimore, Md. : 1950)
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Adhesion molecules, endothelial products, and microalbuminuria in essential hypertension

2001

medicine.medical_specialtyEndotheliumbiologybusiness.industryCell adhesion moleculeIntercellular Adhesion Molecule-1Essential hypertensionmedicine.diseaseEndothelin 1medicine.anatomical_structureEndocrinologyInternal medicineE-selectinInternal Medicinemedicinebiology.proteinMicroalbuminuriaEndothelial dysfunctionbusinessAmerican Journal of Hypertension
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Islet beta-cell apoptosis triggered in vivo by interleukin-1beta is not related to the inducible nitric oxide synthase pathway: evidence for mitochon…

2003

IL-1beta is recognized as an effector cytokine contributing to islet beta-cell destruction during diabetes. We have previously shown in vitro that IL-1beta induces nitric oxide (NO) and beta-cell damage. Here, we show that IL-1beta administration in vivo to Wistar rats transiently increases manganese superoxide dismutase activity, whereas inducible NO synthase is not detected, and the levels of nitrate+nitrate do not change. Moreover, a significant decrease of mitochondrial aconitase, leading to a rise of hydroperoxides, and islet beta-cell apoptosis, involving caspase-3 and -8, is observed. Analysis of adhesion molecules in beta-cells showed that intercellular adhesion molecule-1 is highly…

medicine.medical_specialtyLipid PeroxidesNitric Oxide Synthase Type IIApoptosisBiologyMitochondrionIn Vitro TechniquesAconitaseNitric oxidechemistry.chemical_compoundIslets of LangerhansEndocrinologyIn vivoInternal medicinemedicineAnimalsRats WistarNitritesAconitate HydratasegeographyCaspase 8geography.geographical_feature_categoryNitratesCell adhesion moleculeCaspase 3Superoxide DismutaseIsletIntercellular Adhesion Molecule-1Caspase 9Cell biologyMitochondriaRatsNitric oxide synthaseEndocrinologyBiochemistrychemistryApoptosisCaspasesbiology.proteinNitric Oxide SynthaseInterleukin-1Endocrinology
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Effects of Th1 and Th2 cytokines on cytokine production and ICAM-1 expression on synovial fibroblasts

1995

OBJECTIVES--To investigate the influence of the Th1 and Th2 lymphokines interleukins (IL)-4 and IL-13, interferon gamma (IFN gamma), and several monokines on the adhesion of mononuclear cells to synovial fibroblasts and intercellular adhesion molecule-1 (ICAM-1) expression and cytokine production of synovial fibroblasts in patients with osteoarthritis. METHODS--Synovial fibroblasts were isolated from patients with osteoarthritis and stimulated with IL-1 beta, IL-4, IL-6, IL-10, IL-12, IL-13, tumour necrosis factor alpha (TNF alpha), and IFN gamma. Subsequently, we determined the production of IL-1 alpha, IL-1 beta, IL-6, IL-10, IL-12, IFN alpha and TNF alpha, and the expression of ICAM-1 ly…

medicine.medical_treatmentImmunologyIntercellular Adhesion Molecule-1BiologyGeneral Biochemistry Genetics and Molecular BiologyTh2 CellsRheumatologyOsteoarthritisCell AdhesionmedicineHumansImmunology and AllergyInterferon gammaCell adhesionCells CulturedInterleukin-13Interleukin-6Cell adhesion moleculeSynovial MembraneLymphokineReceptors InterleukinFibroblastsTh1 CellsIntercellular Adhesion Molecule-1Molecular biologyRecombinant ProteinsReceptors Interleukin-4Cytokinemedicine.anatomical_structureImmunologyCytokinesTumor necrosis factor alphaInterleukin-4Synovial membraneResearch Articlemedicine.drug
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Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis.

2008

Contains fulltext : 70589.pdf (Publisher’s version ) (Closed access) OBJECTIVE: CO-releasing molecules (CO-RMs) are a novel class of anti-inflammatory agents. We have examined the possible therapeutic effects of CORM-3 in collagen-induced arthritis (CIA). METHODS: Arthritis was induced in DBA-1/J mice by type II collagen. Animals were treated with CORM-3 (5 and 10 mg/kg/day, intraperitoneally) or the inactive compound iCORM-3 (10 mg/kg/day, intraperitoneally) unable to release CO, from days 22 to 31. Production of anti-type II collagen antibodies, cytokines and cartilage olimeric matrix protein (COMP) was evaluated by enzyme-linked immunosorbent assay, and prostaglandin E(2) (PGE(2)) by rad…

musculoskeletal diseasesmedicine.medical_treatmentImmunologyAnti-Inflammatory AgentsDrug Evaluation PreclinicalType II collagenArthritisInflammationPharmacologyAuto-immunity transplantation and immunotherapy [N4i 4]DinoprostoneGeneral Biochemistry Genetics and Molecular BiologyMiceRheumatologyOrganometallic CompoundsPerception and Action [DCN 1]medicineAnimalsImmunology and AllergyChronic inflammation and autoimmunity [UMCN 4.2]Dose-Response Relationship Drugbiologybusiness.industryRANK LigandInterleukinIntercellular Adhesion Molecule-1medicine.diseaseArthritis ExperimentalPathogenesis and modulation of inflammation [N4i 1]Cellular infiltrationCyclooxygenase 2Mice Inbred DBARANKLImmunologybiology.proteinCytokinesTumor necrosis factor alphaMicrobial pathogenesis and host defense [UMCN 4.1]Inflammation Mediatorsmedicine.symptombusinessInfection and autoimmunity [NCMLS 1]Heme Oxygenase-1Immunity infection and tissue repair [NCMLS 1]Prostaglandin E
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