Featured Publications
Differential outcomes of high‐fat diet on age‐related rescaling of cochlear frequency place coding
Zhang Y, Lin G, Xue N, Wang Y, Du T, Liu H, Xiong W, Shang W, Wu H, Song L. Differential outcomes of high‐fat diet on age‐related rescaling of cochlear frequency place coding. The FASEB Journal 2023, 37: e23167. PMID: 37651093, DOI: 10.1096/fj.202300457rr.Peer-Reviewed Original ResearchConceptsAge-related hearing lossHigh-fat dietHearing lossEffects of HFDLoss of OHCsActivation of TRPV1Sensorineural hearing lossCBA/CaJPlace codingCochlear frequency selectivityTRPV1 expressionOHC functionInflammatory responseCommon causeHFD cohortGenetic backgroundYounger ageArachidonic acidCochlear lengthHair cellsPrestin levelsLipid homeostasisRescuing effectCochlear amplificationAge
2023
Role of mitochondrial dysfunction and oxidative stress in sensorineural hearing loss
Tan W, Song L. Role of mitochondrial dysfunction and oxidative stress in sensorineural hearing loss. Hearing Research 2023, 434: 108783. PMID: 37167889, DOI: 10.1016/j.heares.2023.108783.Peer-Reviewed Original ResearchConceptsSensorineural hearing lossOtotoxic drugsMitochondrial dysfunctionReactive oxygen speciesOxidative stressHearing lossDevelopment of SNHLMitochondrial reactive oxygen speciesSpiral ganglion neuronsMitochondrial DNA mutationsPrecise pathophysiological mechanismsSensory hair cellsHair cell mitochondriaConsequent oxidative stressCentral etiological roleMtDNA mutationsPathophysiological mechanismsGanglion neuronsAntioxidant therapyCalcium dysregulationDNA mutationsCell mitochondriaClinical studiesCochlear cellsEtiological role
2022
Prestin-Mediated Frequency Selectivity Does not Cover Ultrahigh Frequencies in Mice
Li J, Liu S, Song C, Zhu T, Zhao Z, Sun W, Wang Y, Song L, Xiong W. Prestin-Mediated Frequency Selectivity Does not Cover Ultrahigh Frequencies in Mice. Neuroscience Bulletin 2022, 38: 769-784. PMID: 35279808, PMCID: PMC9276951, DOI: 10.1007/s12264-022-00839-4.Peer-Reviewed Original ResearchConceptsOuter hair cellsCation channel blockerCochlear outer hair cellsPrestin knockout miceAudiometric measurementsChannel blockersPharmacogenetic manipulationCochlear sensitivityMiceSpecific ablationHair cellsTarget cellsBehavior testsHearingMembrane potentialLow-pass featureAblationUltrasonic hearingCellsPrestinBlockersMembrane resonanceIn vivo CRISPR‐Cas9‐mediated DNA chop identifies a cochlear outer hair cell‐specific enhancer
Sun Y, Zhang Y, Zhang D, Wang G, Song L, Liu Z. In vivo CRISPR‐Cas9‐mediated DNA chop identifies a cochlear outer hair cell‐specific enhancer. The FASEB Journal 2022, 36: e22233. PMID: 35225354, DOI: 10.1096/fj.202100421rr.Peer-Reviewed Original ResearchConceptsDNA fragment deletionKbp fragmentKbp segmentFragment deletionCell-specific enhancerOuter hair cellsLarge DNA fragment deletionGreen fluorescent proteinCRISPR/Motor proteinsIntron regionsGene therapeutic applicationsFluorescent proteinDifferent speciesCochlear outer hair cellsBp fragmentEnhancerSLC26A5Hair cellsEGFPProteinTransgenic miceDeletionKbpPrestin expression
2019
Hearing consequences in Gjb2 knock-in mice: implications for human p.V37I mutation
Lin X, Li G, Zhang Y, Zhao J, Lu J, Gao Y, Liu H, Li G, Yang T, Song L, Wu H. Hearing consequences in Gjb2 knock-in mice: implications for human p.V37I mutation. Aging 2019, 11: 7416-7441. PMID: 31562289, PMCID: PMC6782001, DOI: 10.18632/aging.102246.Peer-Reviewed Original ResearchConceptsHomozygous miceLate-onset progressive hearing lossV37I mutationABR wave I latencySpiral ganglion neuron lossOuter hair cell functionSignificant hair cell lossMiddle ear injectionStria vascularis atrophyWave I latencyABR threshold elevationsProgressive hearing lossHair cell lossHair cell functionEnvironmental insultsI latencyNeuron lossCochlear pathologyHearing lossEar injectionMouse modelCell lossNoise exposureSystemic applicationThreshold elevation
2017
Novel Role of the Mitochondrial Protein Fus1 in Protection from Premature Hearing Loss via Regulation of Oxidative Stress and Nutrient and Energy Sensing Pathways in the Inner Ear
Tan WJ, Song L, Graham M, Schettino A, Navaratnam D, Yarbrough WG, Santos-Sacchi J, Ivanova AV. Novel Role of the Mitochondrial Protein Fus1 in Protection from Premature Hearing Loss via Regulation of Oxidative Stress and Nutrient and Energy Sensing Pathways in the Inner Ear. Antioxidants & Redox Signaling 2017, 27: 489-509. PMID: 28135838, PMCID: PMC5564041, DOI: 10.1089/ars.2016.6851.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcysteineAnimalsAntioxidantsDisease Models, AnimalEar, InnerEvoked Potentials, Auditory, Brain StemGene Knockout TechniquesHearing LossHumansMiceMicroscopy, Electron, TransmissionMitochondriaOxidative StressProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionSpiral GanglionTOR Serine-Threonine KinasesTumor Suppressor ProteinsConceptsAge-related hearing lossAuditory brainstem responseHearing lossKO miceEndocochlear potentialOxidative stressMitochondrial dysfunctionMitochondrial dysfunction/oxidative stressEnergy sensing pathwaysNovel therapeutic strategiesMolecular mechanismsPremature hearing lossCochlear stria vascularisMajor hearing lossChronic mitochondrial dysfunctionMetabolic etiologyWorldwide epidemicBrainstem responseClinical trialsVascular pathologyTherapeutic strategiesPathological alterationsABR parametersAO treatmentStria vascularis
2012
Mitochondrial Stress Engages E2F1 Apoptotic Signaling to Cause Deafness
Raimundo N, Song L, Shutt TE, McKay SE, Cotney J, Guan MX, Gilliland TC, Hohuan D, Santos-Sacchi J, Shadel GS. Mitochondrial Stress Engages E2F1 Apoptotic Signaling to Cause Deafness. Cell 2012, 148: 716-726. PMID: 22341444, PMCID: PMC3285425, DOI: 10.1016/j.cell.2011.12.027.Peer-Reviewed Original ResearchConceptsAltered reactive oxygen speciesReactive oxygen speciesMitochondrial ribosome functionMitochondrial disease modelTranscription factor E2F1Tissue-specific pathologyROS-dependent activationRibosome functionRRNA methylationMitochondrial stressApoptotic signalingTissue specificityMtDNA mutationsMetabolic signalingAMP kinaseMultiple tissuesMitochondrial dysfunctionOxygen speciesE2F1MethylationSignalingG cellsEnvironmental factorsApoptosisMice exhibit