0000000000174364

AUTHOR

Wim B. Van Den Berg

showing 4 related works from this author

The CO-releasing molecule CORM-3 protects against articular degradation in the K/BxN serum transfer arthritis model.

2010

Contains fulltext : 89015.pdf (Publisher’s version ) (Closed access) Carbon monoxide-releasing molecules can counteract inflammatory responses. The aim of this study was to investigate whether tricarbonylchloro(glycinate)ruthenium (II) (CORM-3) is able to control the effector phase of experimental arthritis. Arthritis was induced in C57Black-6 mice by an intraperitoneal injection of serum from arthritic K/BxN mice. CORM-3 was administered intraperitoneally at 10 mg/kg/day (5 mg/kg twice a day) from days 0 to 10 and animals were sacrificed on day 11. Serum levels of osteocalcin and prostanoids were measured by enzyme-linked immunosorbent assay and radioimmunoassay. Gene expression was determ…

Cartilage ArticularMaleSerummedicine.medical_specialtymedicine.medical_treatmentIntraperitoneal injectionArthritisMice TransgenicHMGB1Auto-immunity transplantation and immunotherapy [N4i 4]RutheniumMicechemistry.chemical_compoundMice Inbred NODInternal medicineOrganometallic CompoundsmedicineAnimalsPharmacologyCarbon MonoxidebiologyChemistryProstaglandin D2 synthaseRadioimmunoassaymedicine.diseaseArthritis ExperimentalMice Inbred C57BLDisease Models AnimalEndocrinologyRANKLbiology.proteinOsteocalcinProstaglandin D2Infection and autoimmunity [NCMLS 1]European Journal of Pharmacology
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Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
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Influence of heme oxygenase 1 modulation on the progression of murine collagen-induced arthritis.

2005

Contains fulltext : 48023.pdf (Publisher’s version ) (Closed access) OBJECTIVE: Heme oxygenase 1 (HO-1) can be induced by inflammatory mediators as an adaptive response. The objective of the present study was to determine the consequences of HO-1 modulation in the murine collagen-induced arthritis (CIA) model. METHODS: DBA/1J mice were treated with an inhibitor of HO-1, tin protoporphyrin IX (SnPP), or with an inducer of HO-1, cobalt protoporphyrin IX (CoPP), from day 22 to day 29 after CIA induction. The clinical evolution of disease was monitored visually. At the end of the experiment, joints were examined for histopathologic changes. Cytokine levels in paws were measured by enzyme-linked…

Metalloporphyrinsmedicine.medical_treatmentImmunologyArthritisProtoporphyrinsInflammationPharmacologyAuto-immunity transplantation and immunotherapy [N4i 4]MiceRheumatologyFibrosismedicinePerception and Action [DCN 1]Immunology and AllergyAnimalsPharmacology (medical)Enzyme InhibitorsChronic inflammation and autoimmunity [UMCN 4.2]biologybusiness.industryMembrane Proteinsmedicine.diseaseCOPPArthritis ExperimentalHeme oxygenaseEnzyme ActivationPathogenesis and modulation of inflammation [N4i 1]Disease Models AnimalCytokineCyclooxygenase 2Mice Inbred DBAProstaglandin-Endoperoxide SynthasesImmunologyChronic DiseaseHeme Oxygenase (Decyclizing)biology.proteinDisease ProgressionTumor necrosis factor alphaJointsCyclooxygenasemedicine.symptombusinessInfection and autoimmunity [NCMLS 1]Heme Oxygenase-1
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Chronic skin inflammation leads to bone loss by IL-17-mediated inhibition of Wnt signaling in osteoblasts

2016

Item does not contain fulltext Inflammation has important roles in tissue regeneration, autoimmunity, and cancer. Different inflammatory stimuli can lead to bone loss by mechanisms that are not well understood. We show that skin inflammation induces bone loss in mice and humans. In psoriasis, one of the prototypic IL-17A-mediated inflammatory human skin diseases, low bone formation and bone loss correlated with increased serum IL-17A levels. Similarly, in two mouse models with chronic IL-17A-mediated skin inflammation,K14-IL17A(ind)andJunB(Deltaep), strong inhibition of bone formation was observed, different from classical inflammatory bone loss where osteoclast activation leads to bone deg…

0301 basic medicineMaleInflammationModels BiologicalOsteocytesBone resorptionEpithelium03 medical and health sciences0302 clinical medicineOsteoclastOsteogenesismedicineAnimalsHumansPsoriasisCell LineageBone ResorptionWnt Signaling PathwaySkin030203 arthritis & rheumatologyInflammationOsteoblastsChemistryInnate lymphoid cellInterleukin-17Wnt signaling pathwayOsteoblastGeneral MedicineMiddle AgedMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression RegulationOsteocyteImmunologyChronic DiseaseCancer researchFemaleInterleukin 17medicine.symptomInflammatory diseases Radboud Institute for Molecular Life Sciences [Radboudumc 5]Science Translational Medicine
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