2024
Exploring a Novel Role of Glycerol Kinase 1 in Prostate Cancer PC-3 Cells
Park B, Kim S, Yu S, Kim K, Jeon H, Ahn S. Exploring a Novel Role of Glycerol Kinase 1 in Prostate Cancer PC-3 Cells. Biomolecules 2024, 14: 997. PMID: 39199385, PMCID: PMC11352368, DOI: 10.3390/biom14080997.Peer-Reviewed Original ResearchPC-3 cellsProstate cancer PC-3 cellsGK deficiencyCell deathProstate cancerAnti-cancer agentsKinase 1Apoptotic cell deathDNA microarray analysisHuman prostate cancer PC-3 cellsCancer cell deathModulating tumor microenvironmentProstate cancer cellsBiomarkers of cell deathX chromosomeReduced cell viabilityEpigenetic regulationExpression vectorInvestigated genesSynthesis of triglyceridesMicroarray analysisGenetic alterationsTumor microenvironmentNovel roleCancer cellsStem cell migration drives lung repair in living mice
Chioccioli M, Liu S, Magruder S, Tata A, Borriello L, McDonough J, Konkimalla A, Kim S, Nouws J, Gonzalez D, Traub B, Ye X, Yang T, Entenberg D, Krishnaswamy S, Hendry C, Kaminski N, Tata P, Sauler M. Stem cell migration drives lung repair in living mice. Developmental Cell 2024, 59: 830-840.e4. PMID: 38377991, PMCID: PMC11003834, DOI: 10.1016/j.devcel.2024.02.003.Peer-Reviewed Original ResearchStem cell migrationCell migrationAlveolar type 2 cellsAlveolar unitsStem cell motilityAlveolar type 1 cellsStem cell activityCellular response to injuryResponse to injuryType 2 cellsMotile phenotypeType 1 cellsCell motilityLung repairImpaired regenerationGenetic depletionCell activationAT2Stem cellsTissue repairAT1Longitudinal imagingInjuryMotilityCellular resolution
2023
Investigating rutin as a potential transforming growth factor‐β type I receptor antagonist for the inhibition of bleomycin‐induced lung fibrosis
Karunarathne W, Lee K, Choi Y, Kang C, Lee M, Kim S, Kim G. Investigating rutin as a potential transforming growth factor‐β type I receptor antagonist for the inhibition of bleomycin‐induced lung fibrosis. BioFactors 2023, 50: 477-492. PMID: 38006284, DOI: 10.1002/biof.2020.Peer-Reviewed Original ResearchIdiopathic pulmonary fibrosisEpithelial-mesenchymal transitionPotential of rutinLung fibrosisType I receptor antagonistChronic lung conditionsPotential therapeutic optionTGF-β type I receptorFibrotic signaling pathwaysInhibition of bleomycinSmooth muscle actinNon-toxic concentrationsType I receptorPulmonary fibrosisCancer-related diseasesTherapeutic optionsReceptor antagonistLung conditionsLung fibroblast cellsFibrosisMuscle actinEMT processType 1ECM-related genesTGFVISTA (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 targetBiological characterization of mulberry leaves bioconverted with Viscozyme L
Kim Y, Yu S, Kim K, Kim S, Park B, Oh H, Kim D, Park K, Ahn S. Biological characterization of mulberry leaves bioconverted with Viscozyme L. Molecular & Cellular Toxicology 2023, 19: 817-828. DOI: 10.1007/s13273-023-00350-5.Peer-Reviewed Original ResearchNormal phase silica gelNuclear magnetic resonance spectroscopyActive compoundsPotent α-glucosidase inhibitorsMagnetic resonance spectroscopyΑ-glucosidaseSilica gelΑ-glucosidase inhibitorsEthyl acetate extractionResonance spectroscopyColumn chromatographyCompoundsPH 4Biological activityEnhanced activityPharmaceutical productsCytotoxicity activityXanthine oxidase inhibitory activityBioactive compoundsAnti-diabetic effectsXanthine oxidaseAcetate extractionCaffeic acidAnti-oxidant propertiesInhibitory activity
2022
Concurrent targeting of glycolysis in bacteria and host cell inflammation in septic arthritis
Kwon H, Yu K, Cahill S, Alder K, Dussik C, Kim S, Sharma L, Back J, Oh I, Lee F. Concurrent targeting of glycolysis in bacteria and host cell inflammation in septic arthritis. EMBO Molecular Medicine 2022, 14: emmm202115284. PMID: 36354099, PMCID: PMC9728052, DOI: 10.15252/emmm.202115284.Peer-Reviewed Original ResearchConceptsDrug dimethyl fumarateSeptic arthritisIntracellular MRSABacterial joint infectionSoft tissue infectionsAnti-inflammatory effectsInfection-associated inflammationNovel therapeutic paradigmContext of infectionConventional antibiotic treatmentHost cellsAdjuvant administrationSurgical treatmentTissue infectionsClinical symptomsInflammatory machineryJoint infectionBacterial burdenAntibiotic treatmentCell inflammationHost inflammationArthritisInflammationIntraarticular inflammationTherapeutic paradigmInhibitory Effect of Biotransformed-Fucoidan on the Differentiation of Osteoclasts Induced by Receptor for Activation of Nuclear Factor-κB Ligand
Park B, Yu S, Kim S, Lee J, Choi S, Chang J, Yang E, Kim K, Ahn S. Inhibitory Effect of Biotransformed-Fucoidan on the Differentiation of Osteoclasts Induced by Receptor for Activation of Nuclear Factor-κB Ligand. Journal Of Microbiology And Biotechnology 2022, 32: 1017-1025. PMID: 35879294, PMCID: PMC9628933, DOI: 10.4014/jmb.2203.03001.Peer-Reviewed Original ResearchConceptsNuclear factor-κB ligandBone marrow macrophagesOsteoclast differentiationBone homeostasisBackground of osteoporosisLow molecular weight fucoidanExpression of NFATc1Effect of fucoidanDifferentiation of osteoclastsResistant acid phosphatase activityHarmful side effectsSide effectsPharmaceutical treatmentWeight fucoidanKey transcriptional factorOsteoporosisMarrow macrophagesDifferentiated osteoclastsInhibitory effectOsteoclastsRT-PCRC-fosSafe natural productTreating ‘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 LungMacrophage-preferable delivery of the leucine-rich repeat domain of NLRX1 ameliorates lethal sepsis by regulating NF-κB and inflammasome signaling activation
Koo JH, Kim SH, Jeon SH, Kang MJ, Choi JM. Macrophage-preferable delivery of the leucine-rich repeat domain of NLRX1 ameliorates lethal sepsis by regulating NF-κB and inflammasome signaling activation. Biomaterials 2021, 274: 120845. PMID: 33971559, DOI: 10.1016/j.biomaterials.2021.120845.Peer-Reviewed Original ResearchConceptsSystemic inflammationSepsis modelNF-κBAcute systemic inflammatory diseaseSymptoms of sepsisSystemic inflammatory diseaseAnti-TNFα antibodyIL-6 productionIL-1β productionEffective therapeutic agentCaspase-1 activationOrgan dysfunctionLethal sepsisTreatment optionsInflammatory diseasesP65 phosphorylationSepsisIκB degradationBacterial infectionsPeritoneal macrophagesTherapeutic agentsMacrophagesInflammationInflammasomeLPSPINK1 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
Dual role of reactive oxygen species in autophagy and apoptosis induced by compound PN in prostate cancer cells
Choi H, Kim K, Park K, Kim S, Park S, Yu S, Kim Y, Kim D, Chung K, Ahn S. Dual role of reactive oxygen species in autophagy and apoptosis induced by compound PN in prostate cancer cells. Molecular & Cellular Toxicology 2020, 17: 41-50. DOI: 10.1007/s13273-020-00107-4.Peer-Reviewed Original ResearchMitochondrial reactive oxygen speciesReactive oxygen speciesCell deathMolecular mechanismsProstate cancer cellsPC-3 cellsCell survivalAnti-cancer activityROS productionApoptotic cell deathCancer cellsOxygen speciesROS-dependent mannerInduction of apoptosisProstate cancer PC-3 cellsHuman prostate cancer cellsAcceleration of apoptosisCancer PC-3 cellsInhibition of autophagyProduction of intracellularIntracellular ROS scavengerProstate cancer treatmentExpression of apoptosisAutophagy inductionWestern blot analysisAnti-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 abilityMitochondrial antiviral signaling protein is crucial for the development of pulmonary fibrosis
Kim SH, Lee JY, Yoon CM, Shin HJ, Lee SW, Rosas I, Herzog E, Dela Cruz C, Kaminski N, Kang MJ. Mitochondrial antiviral signaling protein is crucial for the development of pulmonary fibrosis. European Respiratory Journal 2020, 57: 2000652. PMID: 33093124, PMCID: PMC8559259, DOI: 10.1183/13993003.00652-2020.Peer-Reviewed Original ResearchConceptsDamage-associated molecular patternsIdiopathic pulmonary fibrosisPulmonary fibrosisMAVS aggregationMultiple damage-associated molecular patternsExperimental pulmonary fibrosisMitochondrial antiviral signaling proteinInnate immune responseIPF patientsMAVS signalingIPF treatmentBleomycin injuryLung fibrosisTherapeutic effectImmune responseTherapeutic strategiesMAVS expressionFibrosisDanger signalsCritical mediatorMolecular patternsABT-263LungInjuryBH3 mimetics
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
2017
Mitochondrial ROS activates ERK/autophagy pathway as a protected mechanism against deoxypodophyllotoxin-induced apoptosis
Kim SH, Kim KY, Park SG, Yu SN, Kim YW, Nam HW, An HH, Kim YW, Ahn SC. Mitochondrial ROS activates ERK/autophagy pathway as a protected mechanism against deoxypodophyllotoxin-induced apoptosis. Oncotarget 2017, 5: 111581-111596. PMID: 29340076, PMCID: PMC5762344, DOI: 10.18632/oncotarget.22875.Peer-Reviewed Original ResearchMitochondrial reactive oxygen speciesReactive oxygen speciesCell death responseMultiple cellular processesProtein 1 light chain 3Apoptotic prostate cancer cellsSelective fluorescent dyeMicrotubule-associated protein 1 light chain 3Acidic vesicular organellesMitochondrial membrane potentialG2/M cell cycle arrestM cell cycle arrestCell cycle arrestLight chain 3LC3 knockdownCellular processesDeath responseInhibition of autophagyApoptosis-related proteinsVesicular organellesAutophagy pathwayMolecular mechanismsCellular responsesProstate cancer cell linesProstate cancer cellsInhibition of Autophagy Promotes Salinomycin-Induced Apoptosis via Reactive Oxygen Species-Mediated PI3K/AKT/mTOR and ERK/p38 MAPK-Dependent Signaling in Human Prostate Cancer Cells
Kim K, Park K, Kim S, Yu S, Park S, Kim Y, Seo Y, Ma J, Ahn S. Inhibition of Autophagy Promotes Salinomycin-Induced Apoptosis via Reactive Oxygen Species-Mediated PI3K/AKT/mTOR and ERK/p38 MAPK-Dependent Signaling in Human Prostate Cancer Cells. International Journal Of Molecular Sciences 2017, 18: 1088. PMID: 28524116, PMCID: PMC5454997, DOI: 10.3390/ijms18051088.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisAutophagyCell ProliferationExtracellular Signal-Regulated MAP KinasesFlavonoidsHumansImidazolesMaleMAP Kinase Signaling SystemMembrane Potential, MitochondrialP38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktPyransPyridinesReactive Oxygen SpeciesTOR Serine-Threonine KinasesConceptsExtracellular signal-regulated kinasePI3K/Akt/mTORProstate cancer cellsAkt/mTORCancer cellsP38 MAPK-dependent signalingUpregulation of ERKSignal-regulated kinaseMAPK-dependent signalingP38 MAPK signaling pathwaysMitochondrial membrane potentialMAPK signaling pathwaysChemo-resistant cancersHuman prostate cancer cellsReactive oxygen species productionInhibition of autophagyPI3K inhibitorsPotential antitumor mechanismAcridine orange stainingCaspase-3 activityOxygen species productionSignaling pathwaysP38 inhibitorPropidium iodide assayMTOR activity