2024
Stem 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
2020
Mitochondrial 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 mimeticsGenetic determinants of ammonia-induced acute lung injury in mice
Bein K, Ganguly K, Martin TM, Concel VJ, Brant KA, Di YPP, Upadhyay S, Fabisiak JP, Vuga LJ, Kaminski N, Kostem E, Eskin E, Prows DR, Jang AS, Leikauf GD. Genetic determinants of ammonia-induced acute lung injury in mice. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2020, 320: l41-l62. PMID: 33050709, PMCID: PMC7847062, DOI: 10.1152/ajplung.00276.2020.Peer-Reviewed Original ResearchConceptsSNP associationsWide association mappingGenetic determinantsSignificant SNP associationsAcute lung injuryIntegrative functional approachAssociation mappingMolecular functionsTranscriptomic analysisCandidate genesFunctional domainsNonsynonymous SNPsPromoter regionLung injuryDiverse panelGenesSNPsMouse strainsPathophysiological roleAATFInjuryProteinLAMA3ExpressionAssembly
2011
Integrative metabolome and transcriptome profiling reveals discordant energetic stress between mouse strains with differential sensitivity to acrolein‐induced acute lung injury
Fabisiak JP, Medvedovic M, Alexander DC, McDunn JE, Concel VJ, Bein K, Jang AS, Berndt A, Vuga LJ, Brant KA, Pope‐Varsalona H, Dopico RA, Ganguly K, Upadhyay S, Li Q, Hu Z, Kaminski N, Leikauf GD. Integrative metabolome and transcriptome profiling reveals discordant energetic stress between mouse strains with differential sensitivity to acrolein‐induced acute lung injury. Molecular Nutrition & Food Research 2011, 55: 1423-1434. PMID: 21823223, PMCID: PMC3482455, DOI: 10.1002/mnfr.201100291.Peer-Reviewed Original ResearchConceptsAcute lung injuryLung injuryAcrolein exposureMouse lungMouse strainsJ mouse lungEnvironmental tobacco smokeChain amino acid metabolismFatty acid β-oxidationLung metabolomeJ miceSM/J miceTobacco smokeAcrolein treatmentRespiratory irritantsAmino acid metabolismLungEnergetic stressInjuryAcid metabolismSM/JΒ-oxidationMiceIntegrative metabolomeHealth hazardsCytokine-Like Factor I (CLF1) Expression Is Increased In Idiopathic Pulmonary Fibrosis (IPF) And Promotes Inflammation But Decreases Fibrosis In Bleomycin Injury
Kass D, Loh K, Borczuk A, Tedrow J, Guardela B, Kaminski N, Greenberg S. Cytokine-Like Factor I (CLF1) Expression Is Increased In Idiopathic Pulmonary Fibrosis (IPF) And Promotes Inflammation But Decreases Fibrosis In Bleomycin Injury. 2011, a2710-a2710. DOI: 10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2710.Peer-Reviewed Original Research
2010
Functional Genomics of Chlorine-induced Acute Lung Injury in Mice
Leikauf GD, Pope-Varsalona H, Concel VJ, Liu P, Bein K, Brant KA, Dopico RA, Di YP, Jang AS, Dietsch M, Medvedovic M, Li Q, Vuga LJ, Kaminski N, You M, Prows DR. Functional Genomics of Chlorine-induced Acute Lung Injury in Mice. Annals Of The American Thoracic Society 2010, 7: 294-296. PMID: 20601635, PMCID: PMC3136967, DOI: 10.1513/pats.201001-005sm.Peer-Reviewed Original ResearchConceptsAcute lung injuryChlorine-induced acute lung injuryLung injuryMouse strainsMean survival timeGene-targeted miceSusceptibility candidate genesSupportive measuresSurvival timeDivergent strainsInjuryCandidate genesCritical candidate genesFunctional genomics approachMiceAdditional genetic analysesMolecular eventsFunctional significanceFunctional genomicsGenomic approachesChlorine exposureGenetic basisNovel insightsGenetic analysisHospitalizationCandidate Susceptibility Genes Identified By Genomewide Analysis Of Chloride-induced Acute Lung Injury In Mice
Leikauf G, Pope-Varsalona H, Concel V, Liu P, Bein K, Brant K, Dopico R, Di Y, Jang A, Medvedovic M, Li Q, Vega L, Kaminski N, You M, Prows D. Candidate Susceptibility Genes Identified By Genomewide Analysis Of Chloride-induced Acute Lung Injury In Mice. 2010, a5370-a5370. DOI: 10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5370.Peer-Reviewed Original Research
2008
Mitogen-Activated Protein Kinases Regulate Susceptibility to Ventilator-Induced Lung Injury
Dolinay T, Wu W, Kaminski N, Ifedigbo E, Kaynar AM, Szilasi M, Watkins SC, Ryter SW, Hoetzel A, Choi AM. Mitogen-Activated Protein Kinases Regulate Susceptibility to Ventilator-Induced Lung Injury. PLOS ONE 2008, 3: e1601. PMID: 18270588, PMCID: PMC2223071, DOI: 10.1371/journal.pone.0001601.Peer-Reviewed Original ResearchConceptsVentilator-induced lung injuryMatrix metalloproteinase-8Lung injuryInflammatory lung injuryWild-type miceMechanical ventilationProtein kinase kinase 3C57/BL6 wild-type miceLung injury parametersTerminal kinase 1C-JunLung vascular permeabilityProtein kinaseKinase 1Kinase 3Edema formationMitogen-activated protein kinase kinase 3Metalloproteinase-8Vascular permeabilityMitogen-activated protein kinase pathwayInjuryInjury parametersComprehensive gene expression profilingMiceProtein leakage
2007
Approaching the degradome in idiopathic pulmonary fibrosis
Pardo A, Selman M, Kaminski N. Approaching the degradome in idiopathic pulmonary fibrosis. The International Journal Of Biochemistry & Cell Biology 2007, 40: 1141-1155. PMID: 18207447, DOI: 10.1016/j.biocel.2007.11.020.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisIPF lungsProgressive fibrosisEpithelial injuryUnknown etiologyLung disordersBody of evidenceLung fibrogenesisLung parenchymaAbnormal remodelingExaggerated accumulationFibrosisSignificant upregulationExtracellular matrixLungCritical roleGene expression studiesFoci formationGlobal gene expression studiesFibrogenesisPathogenesisInjuryEtiologyParenchyma
2006
Gene expression profiling of target genes in ventilator-induced lung injury
Dolinay T, Kaminski N, Felgendreher M, Kim HP, Reynolds P, Watkins SC, Karp D, Uhlig S, Choi AM. Gene expression profiling of target genes in ventilator-induced lung injury. Physiological Genomics 2006, 26: 68-75. PMID: 16569776, DOI: 10.1152/physiolgenomics.00110.2005.Peer-Reviewed Original ResearchMeSH KeywordsA Kinase Anchor ProteinsAmphiregulinAnimalsCell Cycle ProteinsCluster AnalysisCysteine-Rich Protein 61DNA-Binding ProteinsEGF Family of ProteinsGene Expression ProfilingGene Expression RegulationGlycoproteinsImmediate-Early ProteinsImmunohistochemistryIntercellular Signaling Peptides and ProteinsInterleukin-11LipopolysaccharidesLungLung InjuryMaleMiceMice, Inbred BALB CNuclear Receptor Subfamily 4, Group A, Member 1Oligonucleotide Array Sequence AnalysisReceptors, Cytoplasmic and NuclearReceptors, SteroidReproducibility of ResultsRespiration, ArtificialRNA, MessengerTranscription FactorsConceptsVentilator-induced lung injuryLung injuryAcute respiratory distress syndromeHigh-pressure mechanical ventilationRespiratory distress syndromeHigh-pressure ventilationLow-pressure ventilationClassical inflammatory pathwaysGrowth factor-related genesDistress syndromeMechanical ventilationInflammatory pathwaysLPS treatmentInflammatory responseReal-time PCRMouse lungGene expression profilingProtein expressionImmunoblotting assaysMRNA expression patternsVentilationOverventilationLungNovel candidate genesInjury
2001
TGF-β is a critical mediator of acute lung injury
Pittet J, Griffiths M, Geiser T, Kaminski N, Dalton S, Huang X, Brown L, Gotwals P, Koteliansky V, Matthay M, Sheppard D. TGF-β is a critical mediator of acute lung injury. Journal Of Clinical Investigation 2001, 107: 1537-1544. PMID: 11413161, PMCID: PMC200192, DOI: 10.1172/jci11963.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, NeoplasmBleomycinBlood-Air BarrierCells, CulturedEndotoxinsGlutathioneIntegrinsMiceMice, KnockoutProtein Serine-Threonine KinasesPulmonary AlveoliPulmonary EdemaReceptor, Transforming Growth Factor-beta Type IIReceptors, Transforming Growth Factor betaRespiratory Distress SyndromeTransforming Growth Factor betaConceptsAcute lung injuryPulmonary edemaLung injuryAlveolar epithelial permeabilityWild-type miceEscherichia coli endotoxinColi endotoxinEffective treatmentEpithelial permeabilityIntegrin alphavbeta6Pharmacologic inhibitionEdemaCritical mediatorUntreatable disorderLocal activationIntracellular glutathioneInjuryMiceActivationLungTGFBleomycinEndotoxin