Sang-Hun Kim
Associate Research ScientistCards
About
Research
Publications
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 Lung