2022
Modulators of ASIC1a and its potential as a therapeutic target for age-related diseases
Zhou R, Liang H, Hu W, Ding J, Li S, Chen Y, Zhao Y, Lu C, Chen F, Hu W. Modulators of ASIC1a and its potential as a therapeutic target for age-related diseases. Ageing Research Reviews 2022, 83: 101785. PMID: 36371015, DOI: 10.1016/j.arr.2022.101785.Peer-Reviewed Original ResearchConceptsAcid-sensing ion channel 1aAge-related diseasesTherapeutic targetPotential therapeutic targetMost age-related diseasesIon channel 1aNovel drug targetsEffective drugsMultiple organsPathophysiological processesChannel 1aDiseaseChannel family membersPharmacological propertiesImproved treatmentSuch diseasesTissue degenerationCellular apoptosisTreatmentDrug targetsFamily membersPhysiological functionsUrgent needWorldwide populationIschemia
2019
β-Estradiol Protects Against Acidosis-Mediated and Ischemic Neuronal Injury by Promoting ASIC1a (Acid-Sensing Ion Channel 1a) Protein Degradation
Zhou R, Leng T, Yang T, Chen F, Hu W, Xiong Z. β-Estradiol Protects Against Acidosis-Mediated and Ischemic Neuronal Injury by Promoting ASIC1a (Acid-Sensing Ion Channel 1a) Protein Degradation. Stroke 2019, 50: 2902-2911. PMID: 31412757, PMCID: PMC6756944, DOI: 10.1161/strokeaha.119.025940.Peer-Reviewed Original ResearchConceptsIschemic neuronal injuryIschemic brain injuryΒ-estradiol treatmentASIC1a protein expressionNeuronal injuryASIC currentsBrain injuryProtein expressionΒ-estradiolWhole-cell patch-clamp techniqueIntracellular CaAcidosis-induced cytotoxicityAcidosis-mediated injuryActivation of ASIC1aDegree of neuroprotectionOutcome of strokeSeverity of strokeMiddle cerebral arteryTransient focal ischemiaOnline visual overviewAcid-induced elevationEstrogen receptor αReal-time polymerase chain reactionQuantitative real-time polymerase chain reactionPatch-clamp technique
2018
Acute Ethanol Exposure Promotes Autophagy-Lysosome Pathway-Dependent ASIC1a Protein Degradation and Protects Against Acidosis-Induced Neurotoxicity
Zhou R, Leng T, Yang T, Chen F, Xiong Z. Acute Ethanol Exposure Promotes Autophagy-Lysosome Pathway-Dependent ASIC1a Protein Degradation and Protects Against Acidosis-Induced Neurotoxicity. Molecular Neurobiology 2018, 56: 3326-3340. PMID: 30120732, PMCID: PMC6378129, DOI: 10.1007/s12035-018-1289-0.Peer-Reviewed Original ResearchConceptsAcid-sensing ion channel 1aAutophagy-lysosome pathwayNeuronal cellsAcidosis-induced cytotoxicityAcute ethanol administrationAcute ethanol exposureActivity/expressionEthanol-induced reductionIon channel 1aAutophagy activator rapamycinAutophagy inhibitor CQEffects of ethanolASIC1a expressionIschemic strokeNeuronal injuryAcute treatmentBrain ischemiaNeuroprotective effectsEthanol administrationASIC currentsEthanol exposureTissue acidosisASIC1a channelsChannel 1aNeurotoxicity
2017
ASIC2a overexpression enhances the protective effect of PcTx1 and APETx2 against acidosis-induced articular chondrocyte apoptosis and cytotoxicity
Zhou R, Ni W, Dai B, Wu X, Wang Z, Xie Y, Wang Z, Yang W, Ge J, Hu W, Chen F. ASIC2a overexpression enhances the protective effect of PcTx1 and APETx2 against acidosis-induced articular chondrocyte apoptosis and cytotoxicity. Gene 2017, 642: 230-240. PMID: 29141196, DOI: 10.1016/j.gene.2017.11.034.Peer-Reviewed Original ResearchMeSH KeywordsAcid Sensing Ion Channel BlockersAcid Sensing Ion ChannelsAcidosisAlkanesulfonic AcidsAnimalsApoptosisCells, CulturedChondrocytesCnidarian VenomsCollagen Type IIDrug SynergismGene Expression RegulationGenetic VectorsMAP Kinase Signaling SystemMorpholinesPeptidesPlasmidsRatsSpider VenomsConceptsAcid-sensing ion channel 1aArticular chondrocyte apoptosisChondrocyte apoptosisChondrocyte cytotoxicityRheumatoid arthritisProtective effectExpression of ASIC1aAcidosis-induced injuryERK1/2 MAPK signaling pathwaysIon channel 1aAlone groupNeuroprotective effectsChondroprotective effectsMAPK signaling pathwaysProtective roleType II collagenChannel 1aNeuronal cellsAPETx2ASIC2aPcTx1Phosphorylated ERK1/2Pathological charactersInduced apoptosisII collagenInterleukin-1β and tumor necrosis factor-α augment acidosis-induced rat articular chondrocyte apoptosis via nuclear factor-kappaB-dependent upregulation of ASIC1a channel
Zhou R, Dai B, Xie Y, Wu X, Wang Z, Li Y, Wang Z, Zu S, Ge J, Chen F. Interleukin-1β and tumor necrosis factor-α augment acidosis-induced rat articular chondrocyte apoptosis via nuclear factor-kappaB-dependent upregulation of ASIC1a channel. Biochimica Et Biophysica Acta (BBA) - Molecular Basis Of Disease 2017, 1864: 162-177. PMID: 28986307, DOI: 10.1016/j.bbadis.2017.10.004.Peer-Reviewed Original ResearchConceptsAcid-sensing ion channel 1aIL-1βRheumatoid arthritisInterleukin-1βNF-κB inhibitor ammonium pyrrolidinedithiocarbamateNF-κB DNA-binding activityPrimary articular chondrocytesProinflammatory cytokine interleukin-1βAcidosis-induced cytotoxicityCytokines interleukin-1βTumor necrosis factorImportant pathological characteristicNF-κB pathwayArticular chondrocyte apoptosisCaspase-3/9 expressionIon channel 1aNuclear factor-kappaBPleiotropic biological effectsArticular chondrocytesAgent BAPTA-AMASIC1a expressionChondrocyte cytotoxicityΚB expressionAdjuvant arthritisPathological characteristics