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 targetNLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury
Kim H, Kim M, Kim E, Leem J, Baek S, Lee Y, Kim K, Kang M, Song T, Sohn M. NLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury. Scientific Reports 2023, 13: 3441. PMID: 36859435, PMCID: PMC9975446, DOI: 10.1038/s41598-023-28206-x.Peer-Reviewed Original ResearchConceptsHyperoxic acute lung injuryAcute lung injuryLung injuryWT miceAcute respiratory failurePro-inflammatory cytokinesCell deathRespiratory failureAcute injuryInflammatory cellsReduced mortalityRole of NLRX1Murine modelNLRX1 expressionPro-apoptotic signalingCell cytotoxicityHyperoxiaInjuryMiceProtein leakageHyperoxic conditionsNLRX1Apoptotic cell deathERK 1/2Reactive oxygen species
2021
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
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
2020
Retrograde signaling by a mtDNA-encoded non-coding RNA preserves mitochondrial bioenergetics
Blumental-Perry A, Jobava R, Bederman I, Degar A, Kenche H, Guan B, Pandit K, Perry N, Molyneaux N, Wu J, Prendergas E, Ye Z, Zhang J, Nelson C, Ahangari F, Krokowski D, Guttentag S, Linden P, Townsend D, Miron A, Kang M, Kaminski N, Perry Y, Hatzoglou M. Retrograde signaling by a mtDNA-encoded non-coding RNA preserves mitochondrial bioenergetics. Communications Biology 2020, 3: 626. PMID: 33127975, PMCID: PMC7603330, DOI: 10.1038/s42003-020-01322-4.Peer-Reviewed Original ResearchConceptsMitochondrial genomeNuclear-encoded genesCell type-specific mannerNon-coding RNASteady-state transcriptionMitochondrial energy metabolismControl regionPositive regulationMitochondrial bioenergeticsMitochondria stressMitochondrial functionSpecific mannerAlveolar epithelial type II cellsEnergy metabolismType II cellsEpithelial type II cellsGenomePhysiological stressRNAII cellsCellsMouse lungTranscriptionGenesMitochondriaSmoking Alters Inflammation and Skeletal Stem and Progenitor Cell Activity During Fracture Healing in Different Murine Strains
Hao Z, Li J, Li B, Alder KD, Cahill SV, Munger AM, Lee I, Kwon H, Back J, Xu S, Kang M, Lee FY. Smoking Alters Inflammation and Skeletal Stem and Progenitor Cell Activity During Fracture Healing in Different Murine Strains. Journal Of Bone And Mineral Research 2020, 36: 186-198. PMID: 32866293, PMCID: PMC9057220, DOI: 10.1002/jbmr.4175.Peer-Reviewed Original ResearchConceptsCigarette smoke exposureCigarette smokingFracture healingSmoke exposureMurine modelMolecular alterationsBALB/cJ miceBiomechanical testingPro-inflammatory mediatorsCytokine/chemokine analysisImpaired fracture healingMultiplex cytokine/chemokine analysisInitial inflammatory responseFracture healing capacityBALB/cJProgenitor cell activitySmoking miceTransverse femoral osteotomyFemoral osteotomyImmune cellsChemokine analysisInflammatory responseFracture hematomaHigh riskMurine strains
2010
Transgenic modelling of cytokine polarization in the lung
Dela Cruz CS, Kang M, Cho W, Lee CG. Transgenic modelling of cytokine polarization in the lung. Immunology 2010, 132: 9-17. PMID: 21091906, PMCID: PMC3015070, DOI: 10.1111/j.1365-2567.2010.03376.x.Peer-Reviewed Original ResearchConceptsCytokine polarizationT helper type 17 cytokinesT helper type 2T helper type 1Type 1Type 17 cytokinesHelper type 2Type 2 cytokinesHelper type 1Human lung diseasesVariety of cytokinesCytokine milieuPulmonary inflammationEnvironmental allergensLung diseaseTissue phenotypeInjury modelT-betCommon siteCertain cytokinesEffector functionsTransgenic miceIndividual cytokinesPathophysiological consequencesType 2Th2 LCR is essential for regulation of Th2 cytokine genes and for pathogenesis of allergic asthma
Koh BH, Hwang SS, Kim JY, Lee W, Kang MJ, Lee CG, Park JW, Flavell RA, Lee GR. Th2 LCR is essential for regulation of Th2 cytokine genes and for pathogenesis of allergic asthma. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 10614-10619. PMID: 20483988, PMCID: PMC2890814, DOI: 10.1073/pnas.1005383107.Peer-Reviewed Original ResearchConceptsCD4 T cellsAllergic asthmaTh2 cytokine genesCytokine genesKO miceT cellsNaïve CD4 T cellsLung airway inflammationSerum IgE levelsBronchoalveolar lavage fluidRecruitment of eosinophilsWild-type miceAirway hyperresponsivenessOvalbumin challengeAirway inflammationIgE levelsLavage fluidTh2 cytokinesAirway wallMucus productionMouse modelAsthmaMarked reductionCre-loxP recombinationMice