2020
Nerve growth factor promotes ASIC1a expression via the NF-κB pathway and enhances acid-induced chondrocyte apoptosis
Wei X, Sun C, Zhou R, Ma G, Yang Y, Lu C, Hu W. Nerve growth factor promotes ASIC1a expression via the NF-κB pathway and enhances acid-induced chondrocyte apoptosis. International Immunopharmacology 2020, 82: 106340. PMID: 32146316, DOI: 10.1016/j.intimp.2020.106340.Peer-Reviewed Original ResearchNerve growth factorNF-κB p65 activationMediators of inflammationNF-κB p65Cleaved-PARP expressionNF-κB inhibitorArticular chondrocytesApoptotic protein expressionASIC1a expressionTime-dependent fashionNeurotrophic factorP65 activationNF-κBNervous systemAcid-induced apoptosisLDH releaseChondrocyte apoptosisRat chondrocytesGrowth factorProtein expressionCell viabilityApoptosisChondrocytesExpressionInflammation17β-estradiol attenuates rat articular chondrocyte injury by targeting ASIC1a-mediated apoptosis
Song S, Tao J, Li S, Qian X, Niu R, Wang C, Zhang Y, Chen Y, Wang K, Zhu F, Zhu C, Ma G, Yang-Yang, Peng X, Zhou R, Chen F. 17β-estradiol attenuates rat articular chondrocyte injury by targeting ASIC1a-mediated apoptosis. Molecular And Cellular Endocrinology 2020, 505: 110742. PMID: 32006608, DOI: 10.1016/j.mce.2020.110742.Peer-Reviewed Original ResearchConceptsAcid-sensing ion channel 1aRheumatoid arthritisChondrocyte injuryTreatment of RAEstradiol replacement therapyProtein levelsAcid-induced damageIon channel 1aAutophagy-lysosomal pathwayJoint swellingCartilage destructionLocal inflammationOvariectomized modelReplacement therapyEstrogen metabolismArticular damageEpidemiological evidenceASIC1a proteinProtective roleAcid-induced apoptosisChannel 1aSodium-permeable channelsInjuryERα receptorMitochondrial function
2015
Interleukin-6 enhances acid-induced apoptosis via upregulating acid-sensing ion channel 1a expression and function in rat articular chondrocytes
Zhou R, Wu X, Wang Z, Ge J, Chen F. Interleukin-6 enhances acid-induced apoptosis via upregulating acid-sensing ion channel 1a expression and function in rat articular chondrocytes. International Immunopharmacology 2015, 29: 748-760. PMID: 26359543, DOI: 10.1016/j.intimp.2015.08.044.Peer-Reviewed Original ResearchMeSH KeywordsAcid Sensing Ion ChannelsAcidsAnimalsAntibodies, Monoclonal, HumanizedApoptosisApoptosis Regulatory ProteinsArthritis, ExperimentalCartilage, ArticularChondrocytesDose-Response Relationship, DrugEnzyme ActivationInterleukin-6L-Lactate DehydrogenaseMalePeptidesRatsRats, Sprague-DawleySpider VenomsUp-RegulationConceptsInflammatory cytokine interleukin-6Acid-sensing ion channelsArticular chondrocyte apoptosisRat articular chondrocytesChondrocyte apoptosisRheumatoid arthritisAcid-induced cell injuryArticular chondrocytesAdjuvant arthritis ratsPrimary rat articular chondrocytesChronic inflammatory diseaseCytokine interleukin-6IL-6 receptorJAK2/STAT3Dose-dependent mannerArthritis ratsInflammatory diseasesInterleukin-6Specific antagonistCell injuryNF-κBAcid-induced apoptosisLDH releaseArthritic cartilageDownregulated expression