2023
VISTA (PD-1H) Is a Crucial Immune Regulator to Limit Pulmonary Fibrosis.
Kim S, Adams T, Hu Q, Shin H, Chae G, Lee S, Sharma L, Kwon H, Lee F, Park H, Huh W, Manning E, Kaminski N, Sauler M, Chen L, Song J, Kim T, Kang M. VISTA (PD-1H) Is a Crucial Immune Regulator to Limit Pulmonary Fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2023, 69: 22-33. PMID: 36450109, PMCID: PMC10324045, DOI: 10.1165/rcmb.2022-0219oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisImmune regulatorsTherapeutic potentialHuman idiopathic pulmonary fibrosisCrucial immune regulatorsNovel immune regulatorPulmonary fibrosis micePulmonary fibrosis modelNovel therapeutic targetRole of VISTAWild-type littermatesMonocyte-derived macrophagesT lymphocyte lineageVISTA expressionIPF treatmentAntibody treatmentImmune landscapeFibrotic mediatorsLung fibrosisFibrosis miceInflammatory responseFibrosis modelMyeloid populationsTherapeutic target
2022
Treating ‘Septic’ With Enhanced Antibiotics and ‘Arthritis’ by Mitigation of Excessive Inflammation
Kwon HK, Dussik CM, Kim SH, Kyriakides TR, Oh I, Lee FY. Treating ‘Septic’ With Enhanced Antibiotics and ‘Arthritis’ by Mitigation of Excessive Inflammation. Frontiers In Cellular And Infection Microbiology 2022, 12: 897291. PMID: 35755835, PMCID: PMC9218192, DOI: 10.3389/fcimb.2022.897291.Peer-Reviewed Original ResearchConceptsSeptic arthritisBacterial burdenAntibiotic treatmentMurine modelTherapeutic goalsConcurrent antimicrobial therapyDistinct therapeutic goalsGeneration of inflammationMRSA septic arthritisSeptic knee arthritisInflammatory joint conditionsArticular cartilageMitigation of inflammationPost-antibiotic treatmentNovel therapeutic strategiesSeptic arthritis modelArticular cartilage damageEx vivo modelArticular cartilage integrityInflammatory arthritisInhibitors of ERKInflammatory profileMRSA infectionSynovial tissueExcessive inflammation
2021
Distinct Roles of Type I and Type III Interferons during a Native Murine β Coronavirus Lung Infection
Sharma L, Peng X, Qing H, Hilliard BK, Kim J, Swaminathan A, Tian J, Israni-Winger K, Zhang C, Habet V, Wang L, Gupta G, Tian X, Ma Y, Shin HJ, Kim SH, Kang MJ, Ishibe S, Young LH, Kotenko S, Compton S, Wilen CB, Wang A, Dela Cruz CS. Distinct Roles of Type I and Type III Interferons during a Native Murine β Coronavirus Lung Infection. Journal Of Virology 2021, 96: e01241-21. PMID: 34705554, PMCID: PMC8791255, DOI: 10.1128/jvi.01241-21.Peer-Reviewed Original ResearchConceptsType I interferonType III interferonsI interferonIII interferonsCoronavirus infectionInterferon deficiencyViral clearanceViral loadLung infectionType IHealthy young patientsImproved host survivalHost survivalRole of interferonMurine coronavirus infectionMajor health care threatViral burdenYounger patientsEarly diseaseIntranasal routeInterferon treatmentSublethal infectionEarly treatmentLethal infectionTissue injuryNucleotide‐binding domain and leucine‐rich‐repeat‐containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung‐like changes
Shin HJ, Kim S, Park H, Shin M, Kang I, Kang M. Nucleotide‐binding domain and leucine‐rich‐repeat‐containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung‐like changes. Aging Cell 2021, 20: e13410. PMID: 34087956, PMCID: PMC8282248, DOI: 10.1111/acel.13410.Peer-Reviewed Original ResearchConceptsCellular senescenceActivation of mTORNucleotide-binding domainCellular senescence responseReplicative cellular senescenceNLR family membersOrganismal agingCellular physiologyMitochondrial moleculesSenescence responseCellular locationProtein X1Crucial regulatorMechanistic targetMitochondrial functionMolecular hallmarksNLRX1 functionRapamycin (mTOR) activationMitochondrial dysfunctionSenescenceMTORPharmacological inhibitionNLRX1BiologyAging LungPINK1 Inhibits Multimeric Aggregation and Signaling of MAVS and MAVS-Dependent Lung Pathology.
Kim SH, Shin HJ, Yoon CM, Lee SW, Sharma L, Dela Cruz CS, Kang MJ. PINK1 Inhibits Multimeric Aggregation and Signaling of MAVS and MAVS-Dependent Lung Pathology. American Journal Of Respiratory Cell And Molecular Biology 2021, 64: 592-603. PMID: 33577398, PMCID: PMC8086043, DOI: 10.1165/rcmb.2020-0490oc.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsBleomycinEpithelial CellsGene Expression RegulationHEK293 CellsHumansImmunity, InnateInflammasomesInfluenza A virusLungMiceMice, KnockoutMitochondriaNLR Family, Pyrin Domain-Containing 3 ProteinOrthomyxoviridae InfectionsPeroxisomesProtein AggregatesProtein BindingProtein KinasesPulmonary FibrosisSignal TransductionConceptsMAVS aggregationPINK1 deficiencyBimolecular fluorescence complementation analysisAntiviral innate immuneAppropriate cellular functionsKey molecular processesIntracellular signaling pathwaysInnate immune signalingComplementation analysisCellular functionsIntracellular perturbationsImmune signalingSignaling pathwaysPINK1Molecular processesMitochondria dysfunctionMAVSMAVS signalingMurine modelingSignalingFunctional significanceInnate immuneImportant roleRegulationNew role
2020
Anti-Cancer Effects of RAW 264.7 Cells on Prostate Cancer PC-3 Cells.
Nam H, Bae J, Kim Y, An H, Kim S, Kim K, Yu S, Park B, Lee S, Ahn S. Anti-Cancer Effects of RAW 264.7 Cells on Prostate Cancer PC-3 Cells. Annals Of Clinical & Laboratory Science 2020, 50: 739-746. PMID: 33334788.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell CommunicationCell Line, TumorCell MovementCoculture TechniquesCulture Media, ConditionedEpithelial-Mesenchymal TransitionHumansImmunotherapy, AdoptiveLipopolysaccharidesMacrophagesMaleMiceNeoplasm InvasivenessPC-3 CellsProstatic NeoplasmsRAW 264.7 CellsTumor MicroenvironmentConceptsPC-3 cellsAnti-cancer effectsProstate cancer PC-3 cellsCancer PC-3 cellsRAW 264.7 cellsTumor cellsHuman prostate cancer PC-3 cellsEMT-specific markersHigher anti-cancer effectEnzyme-linked immunosorbent assayQuantitative polymerase chain reactionAnti-cancer agentsPolymerase chain reactionImmune cellsInhibitor of metastasisTumor parametersTherapeutic targetingTGF-β2Snail-1Mesenchymal transitionTumor microenvironmentMigration markersWestern blotImmunosorbent assayAngiogenic ability
2018
Impact of Cigarette Smoke Exposure on the Lung Fibroblastic Response after Influenza Pneumonia
Lee SW, Sharma L, Kang YA, Kim SH, Chandrasekharan S, Losier A, Brady V, Bermejo S, Andrews N, Yoon CM, Liu W, Lee JY, Kang MJ, Dela Cruz CS. Impact of Cigarette Smoke Exposure on the Lung Fibroblastic Response after Influenza Pneumonia. American Journal Of Respiratory Cell And Molecular Biology 2018, 59: 770-781. PMID: 30110182, PMCID: PMC6293077, DOI: 10.1165/rcmb.2018-0004oc.Peer-Reviewed Original ResearchConceptsCigarette smoke exposureLungs of miceInfluenza infectionInfluenza virusBAL fluidSmoke exposureGrowth factor-β1 levelsAir-exposed lungsInfluenza-infected miceSignificant lung injuryFibroblastic responseLung-derived fibroblastsProtein-positive cellsGrowth factor-β1Influenza pneumoniaDifferent time pointsLung injurySmoking groupSignificant morbidityCS exposureMurine modelFibrotic responseΒ1 levelsFactor-β1Weight recoverySalinomycin ameliorates oxidative hepatic damage through AMP-activated protein kinase, facilitating autophagy
Kim K, Lee S, Baek S, Lee E, Jang E, Lee J, Ahn S, Chang J, Oh T, Kim S, Ma J, Kim S, Park K, Kim Y. Salinomycin ameliorates oxidative hepatic damage through AMP-activated protein kinase, facilitating autophagy. Toxicology And Applied Pharmacology 2018, 360: 141-149. PMID: 30290169, DOI: 10.1016/j.taap.2018.10.002.Peer-Reviewed Original ResearchConceptsImportance of AMPKMitochondrial dysfunctionAcidic vesicle organellesOxidative stressProtein kinase activationReactive oxygen species productionProtein kinaseAMPK inhibitionKinase activationSevere oxidative stressOxygen species productionLiver injuryMolecular mechanismsIron-induced apoptosisHepatic protectantStreptomyces albusHuman diseasesAMPKCellular mechanismsLC3-IISalinomycin's effectsArachidonic acidMitochondrial impairmentROS productionAnti-cancer agentsDeoxypodophyllotoxin in Anthriscus sylvestris alleviates fat accumulation in the liver via AMP-activated protein kinase, impeding SREBP-1c signal
Kim KY, Park KI, Lee SG, Baek SY, Lee EH, Kim S, Kim SH, Park SG, Yu SN, Oh TW, Kim JH, Kim KJ, Ahn SC, Kim Y. Deoxypodophyllotoxin in Anthriscus sylvestris alleviates fat accumulation in the liver via AMP-activated protein kinase, impeding SREBP-1c signal. Chemico-Biological Interactions 2018, 294: 151-157. PMID: 30148990, DOI: 10.1016/j.cbi.2018.08.025.Peer-Reviewed Original ResearchMeSH KeywordsAMP-Activated Protein KinasesAnimalsApiaceaeBody WeightCholesterolDiet, High-FatDrugs, Chinese HerbalHep G2 CellsHumansHydrocarbons, FluorinatedLipid MetabolismLiverLiver X ReceptorsMaleMiceMice, Inbred C57BLPodophyllotoxinSignal TransductionSterol Regulatory Element Binding Protein 1SulfonamidesTriglyceridesUp-RegulationConceptsSREBP-1c inhibitionLipogenic genesDysregulation of AMPKAnthriscus sylvestrisProtein kinase activationSREBP-1c inductionHigh-fat dietSREBP-1cAcetyl-CoA carboxylaseSterol regulatory elementFatty acid synthaseTranscription factorsProtein kinaseRegulatory elementsStearoyl-CoA desaturase-1X receptor αLiver X receptor αAMPK activationKinase activationRegulatory mechanismsWild chervilOil Red O stainingFat dietAcid synthaseRed O staining