2024
Single-cell RNA-seq analysis of cell-cell communications in human lung reveals a novel role of VEGF-D in acute lung injury
Yuan Y, Sharma L, Tang W, Raredon M, Ahangari F, Khoury J, Wu D, Niklason L, Kaminski N. Single-cell RNA-seq analysis of cell-cell communications in human lung reveals a novel role of VEGF-D in acute lung injury. Physiology 2024, 39: 1314. DOI: 10.1152/physiol.2024.39.s1.1314.Peer-Reviewed Original ResearchIdiopathic pulmonary fibrosisAcute lung injuryChronic obstructive pulmonary diseaseAcute respiratory distress syndromeAnalysis of cell-cell communicationVEGF-DMicrovascular nicheSingle-cell RNA-seqLung injury modelSingle-cell RNA-seq analysisLung injuryCell-cell communicationLigand-receptor pairsLPS-induced lung injury modelRNA-seqAdjacent cell typesPulmonary diseaseInjury modelHuman lung endothelial cellsBarrier functionImmune cell infiltrationTumor necrosis factor-aRespiratory distress syndromeLung vascular integrityGene expressionDedifferentiated early postnatal lung myofibroblasts redifferentiate in adult disease
Chandran R, Adams T, Kabir I, Gallardo-Vara E, Kaminski N, Gomperts B, Greif D. Dedifferentiated early postnatal lung myofibroblasts redifferentiate in adult disease. Frontiers In Cell And Developmental Biology 2024, 12: 1335061. PMID: 38572485, PMCID: PMC10987733, DOI: 10.3389/fcell.2024.1335061.Peer-Reviewed Original ResearchRNA sequencing analysisSMA+ myofibroblastsGene expression profilesLung myofibroblastsAdult lungSequence analysisResponse to lung injurySingle cell RNA sequencing analysisTissue remodeling genesSmooth muscle cell markersLung to hypoxiaExpression profilesRemodeling genesMuscle cell markersResponse to injuryCell typesSMA cellsLineage tracingLung injuryCell markersLineagesGenesAdult diseaseDrug bleomycinLung surface areaAnti-inflammatory roles of type I interferon signaling in the lung
Feng J, Liu Y, Kim J, Ahangari F, Kaminski N, Bain W, Jie Z, Dela Cruz C, Sharma L. Anti-inflammatory roles of type I interferon signaling in the lung. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2024, 326: l551-l561. PMID: 38375579, PMCID: PMC11380987, DOI: 10.1152/ajplung.00353.2023.Peer-Reviewed Original ResearchType I interferon signalingIfnar1-/- miceI interferon signalingInflammatory cell responseInflammatory responseIfnar1-/-Bleomycin injuryCell responsesWild-type miceBroncho-alveolar lavageElevated inflammatory responsePersistent inflammatory responseChemotherapeutic agent bleomycinAnti-inflammatory roleClinically relevant stimuliAnti-inflammatory mechanismsMyeloid cellsPersistent inflammationLung injuryFibrotic remodelingBacterial clearanceRIG-I signalingNOD-like receptor signalingLung tissueReceptor signaling
2023
Thyroid hormone modulates hyperoxic neonatal lung injury and mitochondrial function
Vamesu B, Nicola T, Li R, Hazra S, Matalon S, Kaminski N, Ambalavanan N, Kandasamy J. Thyroid hormone modulates hyperoxic neonatal lung injury and mitochondrial function. JCI Insight 2023, 8: e160697. PMID: 36917181, PMCID: PMC10243814, DOI: 10.1172/jci.insight.160697.Peer-Reviewed Original ResearchConceptsUmbilical cord-derived mesenchymal stem cellsNeonatal lung injuryMild bronchopulmonary dysplasiaSevere bronchopulmonary dysplasiaBronchopulmonary dysplasiaLung injuryELBW infantsThyroid hormonesLung homogenatesMitochondrial dysfunctionTotal T4Newborn miceLow birth weight infantsMitochondrial functionNeonatal hyperoxic lung injuryPeroxisome proliferator-activated receptor γ coactivator 1αProliferator-activated receptor γ coactivator 1αHyperoxic lung injuryReceptor γ coactivator 1αLow total T4Murine lung fibroblastsΓ coactivator 1αNeonatal hypothyroxinemiaWeight infantsPulmonary fibrosis
2021
A Pulmonary Vascular Model From Endothelialized Whole Organ Scaffolds
Yuan Y, Leiby KL, Greaney AM, Raredon MSB, Qian H, Schupp JC, Engler AJ, Baevova P, Adams TS, Kural MH, Wang J, Obata T, Yoder MC, Kaminski N, Niklason LE. A Pulmonary Vascular Model From Endothelialized Whole Organ Scaffolds. Frontiers In Bioengineering And Biotechnology 2021, 9: 760309. PMID: 34869270, PMCID: PMC8640093, DOI: 10.3389/fbioe.2021.760309.Peer-Reviewed Original ResearchVascular diseaseEndothelial phenotypeLung vascular diseaseAcute lung injuryPulmonary microvascular functionWhole lung scaffoldsVascular barrier functionLung injuryMicrovascular functionEndothelial cell coverageSingle-cell RNA-sequencing analysisLPS treatmentProinflammatory signalsWhole lungLung endotheliumLung systemVascular barrierOrgan engineering approachesBarrier functionLungWhole-organ scaffoldsVascular structuresDrug mechanismsEndotheliumDiseasePINK1 mediates the protective effects of thyroid hormone T3 in hyperoxia-induced lung injury
Zhang Y, Yu G, Kaminski N, Lee P. PINK1 mediates the protective effects of thyroid hormone T3 in hyperoxia-induced lung injury. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2021, 320: l1118-l1125. PMID: 33851544, PMCID: PMC8285622, DOI: 10.1152/ajplung.00598.2020.Peer-Reviewed Original ResearchConceptsLung injuryWT miceThyroid hormonesBronchoalveolar lavageHyperoxia exposureBAL total cell countT3 pretreatmentAdult wild-type miceAdministration of PTULung cellular infiltratesAcute lung injuryWild-type miceNovel protective roleRespiratory failureCellular infiltrateThyroid hormone T3Total cell countHistological changesProtective effectPotential therapyProtective roleCell countCytoprotective effectsMitochondrial injuryHyperoxia
2020
Genetic 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 roleAATFInjuryProteinLAMA3ExpressionAssemblySARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues
Ziegler C, Allon S, Nyquist S, Mbano I, Miao V, Tzouanas C, Cao Y, Yousif A, Bals J, Hauser B, Feldman J, Muus C, Wadsworth M, Kazer S, Hughes T, Doran B, Gatter G, Vukovic M, Taliaferro F, Mead B, Guo Z, Wang J, Gras D, Plaisant M, Ansari M, Angelidis I, Adler H, Sucre J, Taylor C, Lin B, Waghray A, Mitsialis V, Dwyer D, Buchheit K, Boyce J, Barrett N, Laidlaw T, Carroll S, Colonna L, Tkachev V, Peterson C, Yu A, Zheng H, Gideon H, Winchell C, Lin P, Bingle C, Snapper S, Kropski J, Theis F, Schiller H, Zaragosi L, Barbry P, Leslie A, Kiem H, Flynn J, Fortune S, Berger B, Finberg R, Kean L, Garber M, Schmidt A, Lingwood D, Shalek A, Ordovas-Montanes J, Network H, Banovich N, Barbry P, Brazma A, Desai T, Duong T, Eickelberg O, Falk C, Farzan M, Glass I, Haniffa M, Horvath P, Hung D, Kaminski N, Krasnow M, Kropski J, Kuhnemund M, Lafyatis R, Lee H, Leroy S, Linnarson S, Lundeberg J, Meyer K, Misharin A, Nawijn M, Nikolic M, Ordovas-Montanes J, Pe’er D, Powell J, Quake S, Rajagopal J, Tata P, Rawlins E, Regev A, Reyfman P, Rojas M, Rosen O, Saeb-Parsy K, Samakovlis C, Schiller H, Schultze J, Seibold M, Shalek A, Shepherd D, Spence J, Spira A, Sun X, Teichmann S, Theis F, Tsankov A, van den Berge M, von Papen M, Whitsett J, Xavier R, Xu Y, Zaragosi L, Zhang K. SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues. Cell 2020, 181: 1016-1035.e19. PMID: 32413319, PMCID: PMC7252096, DOI: 10.1016/j.cell.2020.04.035.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAlveolar Epithelial CellsAngiotensin-Converting Enzyme 2AnimalsBetacoronavirusCell LineCells, CulturedChildCoronavirus InfectionsCOVID-19EnterocytesGoblet CellsHIV InfectionsHumansInfluenza, HumanInterferon Type ILungMacaca mulattaMiceMycobacterium tuberculosisNasal MucosaPandemicsPeptidyl-Dipeptidase APneumonia, ViralReceptors, VirusSARS-CoV-2Serine EndopeptidasesSingle-Cell AnalysisTuberculosisUp-RegulationConceptsSARS-CoV-2Interferon-stimulated genesAirway epithelial cellsCell subsetsSingle-cell RNA sequencing datasetsRNA sequencing datasetsSARS-CoV-2 receptor ACE2Human interferon-stimulated genesTransmembrane serine protease 2Human airway epithelial cellsEpithelial cellsSevere acute respiratory syndrome coronavirus clade 2SARS-CoV-2 spike proteinType II pneumocytesSerine protease 2Clade 2Putative targetsNon-human primatesSpecific cell subsetsCo-expressing cellsDisease COVID-19ACE2 expressionLung injuryLung type II pneumocytesAbsorptive enterocytes
2017
Modified mesenchymal stem cells using miRNA transduction alter lung injury in a bleomycin model
Huleihel L, Sellares J, Cardenes N, Álvarez D, Faner R, Sakamoto K, Yu G, Kapetanaki MG, Kaminski N, Rojas M. Modified mesenchymal stem cells using miRNA transduction alter lung injury in a bleomycin model. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2017, 313: l92-l103. PMID: 28385811, PMCID: PMC5538868, DOI: 10.1152/ajplung.00323.2016.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersBleomycinBone Marrow CellsCollagenCytokinesDisease Models, AnimalFemaleGene Expression RegulationGene Regulatory NetworksHumansInterleukin-6Leukocyte Common AntigensLung InjuryMesenchymal Stem Cell TransplantationMesenchymal Stem CellsMice, Inbred C57BLMicroRNAsRNA, MessengerSurvival AnalysisTransduction, GeneticTransfectionWeight LossConceptsBone marrow-derived mesenchymal stem cellsMesenchymal stem cellsLung fibrosisLate administrationBleomycin modelMiR-154Different preclinical modelsStem cellsCD45-positive cellsMurine bleomycin modelMarrow-derived mesenchymal stem cellsInitial weight lossLower survival rateAshcroft scoreLung injuryBleomycin instillationFibrotic changesCytokine expressionMice groupsLung tissueOH-prolinePreclinical modelsProtective effectTreatment groupsSurvival rateLoss of Twist1 in the Mesenchymal Compartment Promotes Increased Fibrosis in Experimental Lung Injury by Enhanced Expression of CXCL12
Tan J, Tedrow JR, Nouraie M, Dutta JA, Miller DT, Li X, Yu S, Chu Y, Juan-Guardela B, Kaminski N, Ramani K, Biswas PS, Zhang Y, Kass DJ. Loss of Twist1 in the Mesenchymal Compartment Promotes Increased Fibrosis in Experimental Lung Injury by Enhanced Expression of CXCL12. The Journal Of Immunology 2017, 198: 2269-2285. PMID: 28179498, PMCID: PMC5337810, DOI: 10.4049/jimmunol.1600610.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisIPF patientsLung injuryPulmonary fibrosisT cellsFibrotic lung injuryIPF lung fibroblastsExperimental lung injuryT-cell pathwayApoptosis-resistant fibroblastsMatrix-producing cellsChemoattractant CXCL12Exaggerated fibrosisIPF phenotypeCollagen-producing cellsTranscription factor Twist1Prosurvival phenotypeFibrosisTwist1 expressionIncreased expressionLung fibroblastsCXCL12Low expressionHigh expressionCell pathways
2016
P049 Loss of Twist1 in Colα2(I)+ Cells Promotes Increased Fibrosis in Experimental Lung Injury Through C-X-C Motif Ligand 12 (CXCL12)
Tan J, Tedrow J, Nouraie M, Dutta J, Chu Y, Ramani K, Biswas P, Juan-guardela B, Kaminski N, Zhang Y, Kass D. P049 Loss of Twist1 in Colα2(I)+ Cells Promotes Increased Fibrosis in Experimental Lung Injury Through C-X-C Motif Ligand 12 (CXCL12). QJM 2016, 109: s37-s38. DOI: 10.1093/qjmed/hcw124.021.Peer-Reviewed Original Research
2014
C-X-C Motif Chemokine 13 (CXCL13) Is a Prognostic Biomarker of Idiopathic Pulmonary Fibrosis
Vuga LJ, Tedrow JR, Pandit KV, Tan J, Kass DJ, Xue J, Chandra D, Leader JK, Gibson KF, Kaminski N, Sciurba FC, Duncan SR. C-X-C Motif Chemokine 13 (CXCL13) Is a Prognostic Biomarker of Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 966-974. PMID: 24628285, PMCID: PMC4098096, DOI: 10.1164/rccm.201309-1592oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedAged, 80 and overBiomarkersCase-Control StudiesChemokine CXCL13Disease ProgressionEnzyme-Linked Immunosorbent AssayFemaleHumansIdiopathic Pulmonary FibrosisImmunohistochemistryMaleMiddle AgedOligonucleotide Array Sequence AnalysisPredictive Value of TestsPrognosisPulmonary Disease, Chronic ObstructiveRisk FactorsSensitivity and SpecificitySeverity of Illness IndexConceptsChronic obstructive pulmonary diseaseC motif chemokine 13IPF lungsPrognostic biomarkerB cellsIdiopathic pulmonary fibrosis (IPF) pathogenesisB cell-targeted therapiesAntibody-mediated syndromeDysregulated B cellsPulmonary fibrosis pathogenesisPulmonary artery hypertensionObstructive pulmonary diseaseIdiopathic pulmonary fibrosisSix-month survivalB-cell traffickingAcute exacerbationArtery hypertensionCXCL13 mRNAPlasma CXCL13IPF pathogenesisRespiratory failureLung injuryCXCL13 concentrationsPulmonary diseaseRadiographic emphysemaAging Mesenchymal Stem Cells Fail to Protect Because of Impaired Migration and Antiinflammatory Response
Bustos ML, Huleihel L, Kapetanaki MG, Lino-Cardenas CL, Mroz L, Ellis BM, McVerry BJ, Richards TJ, Kaminski N, Cerdenes N, Mora AL, Rojas M. Aging Mesenchymal Stem Cells Fail to Protect Because of Impaired Migration and Antiinflammatory Response. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 787-798. PMID: 24559482, PMCID: PMC4061541, DOI: 10.1164/rccm.201306-1043oc.Peer-Reviewed Original ResearchConceptsBone marrow-derived MSCsMesenchymal stem cellsChemokine receptorsAcute lung injuryAcute lung diseaseSite of injuryAge-dependent decreaseBone marrow-derived mesenchymal stem cellsMarrow-derived mesenchymal stem cellsInflammatory response genesSuch age-related changesAge-related phenomenonStem cellsAge-related changesAdoptive transferLung injuryEndotoxemic miceLung diseaseAntiinflammatory responseFunctional impairmentMore inflammationProtective effectOld miceParacrine mechanismsAlveolar epitheliumNrf2 Amplifies Oxidative Stress via Induction of Klf9
Zucker SN, Fink EE, Bagati A, Mannava S, Bianchi-Smiraglia A, Bogner PN, Wawrzyniak JA, Foley C, Leonova KI, Grimm MJ, Moparthy K, Ionov Y, Wang J, Liu S, Sexton S, Kandel ES, Bakin AV, Zhang Y, Kaminski N, Segal BH, Nikiforov MA. Nrf2 Amplifies Oxidative Stress via Induction of Klf9. Molecular Cell 2014, 53: 916-928. PMID: 24613345, PMCID: PMC4049522, DOI: 10.1016/j.molcel.2014.01.033.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesBleomycinCell Line, TumorGene Expression RegulationGenes, ReporterHumansKruppel-Like Transcription FactorsLuciferasesLungMiceNF-E2-Related Factor 2NIH 3T3 CellsOxidative StressPromoter Regions, GeneticProtein BindingPulmonary FibrosisReactive Oxygen SpeciesSignal TransductionConceptsReactive oxygen speciesKey transcriptional regulatorMetabolism of ROSOxidative stressPathogenesis of bleomycinKruppel-like factor 9Thioredoxin reductase 2Subsequent cell deathTranscription factor 2Antioxidant gene expressionUbiquitous regulatorsTranscriptional regulatorsIntracellular reactive oxygen speciesLung injuryFeedforward regulationPulmonary fibrosisGene expressionOxidant injuryROS clearanceCell deathReductase 2Mouse tissuesCultured cellsNF-E2Factor 9
2013
Activation of Human Mesenchymal Stem Cells Impacts Their Therapeutic Abilities in Lung Injury by Increasing Interleukin (IL)-10 and IL-1RN Levels
Bustos ML, Huleihel L, Meyer EM, Donnenberg AD, Donnenberg VS, Sciurba JD, Mroz L, McVerry BJ, Ellis BM, Kaminski N, Rojas M. Activation of Human Mesenchymal Stem Cells Impacts Their Therapeutic Abilities in Lung Injury by Increasing Interleukin (IL)-10 and IL-1RN Levels. Stem Cells Translational Medicine 2013, 2: 884-895. PMID: 24089414, PMCID: PMC3808203, DOI: 10.5966/sctm.2013-0033.Peer-Reviewed Original ResearchConceptsAcute respiratory distress syndromeAnti-inflammatory effectsBone marrow aspirateReceptor antagonistMarrow aspiratesMesenchymal stem cellsBronchoalveolar lavage inflammatory cellsIL-1 receptor antagonistHuman mesenchymal stem cellsLung injury scoreRespiratory distress syndromeAnti-inflammatory capacityExpression of interleukinStem cellsARDS patientsLung inflammationLung injuryDistress syndromeEndotoxemic micePulmonary edemaInflammatory cellsInjury scoreClinical trialsEffective therapyImmunomodulatory phenotypeSyndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling
Shi Y, Gochuico BR, Yu G, Tang X, Osorio JC, Fernandez IE, Risquez CF, Patel AS, Shi Y, Wathelet MG, Goodwin AJ, Haspel JA, Ryter SW, Billings EM, Kaminski N, Morse D, Rosas IO. Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling. American Journal Of Respiratory And Critical Care Medicine 2013, 188: 831-841. PMID: 23924348, PMCID: PMC3826270, DOI: 10.1164/rccm.201303-0434oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBleomycinBronchoalveolar LavageCaveolin 1Disease Models, AnimalGene Expression ProfilingGenetic MarkersHumansHydroxyprolineIdiopathic Pulmonary FibrosisIn Vitro TechniquesMacrophages, AlveolarMiceMice, TransgenicSignal TransductionSyndecan-2Tissue Array AnalysisTransforming Growth Factor beta1Up-RegulationConceptsHuman syndecan-2TGF-β1 target genesSyndecan-2Target genesIdiopathic pulmonary fibrosisEpithelial cell apoptosisAlveolar epithelial cellsEpithelial cellsTransforming Growth Factor-β1 SignalingCell apoptosisAntifibrotic effectsTGF-β1TGF-β signalingLung injuryPulmonary fibrosisAlveolar epithelial cell apoptosisExtracellular matrix productionTransgenic miceGrowth factor-β1 (TGF-β1) signalingMacrophage-specific overexpressionLung fibrosisMicroarray assayΒ1 signalingAlveolar macrophagesDownstream expression
2012
Matrix Metalloproteinase-19 Is a Key Regulator of Lung Fibrosis in Mice and Humans
Yu G, Kovkarova-Naumovski E, Jara P, Parwani A, Kass D, Ruiz V, Lopez-Otín C, Rosas IO, Gibson KF, Cabrera S, Ramírez R, Yousem SA, Richards TJ, Chensny LJ, Selman M, Kaminski N, Pardo A. Matrix Metalloproteinase-19 Is a Key Regulator of Lung Fibrosis in Mice and Humans. American Journal Of Respiratory And Critical Care Medicine 2012, 186: 752-762. PMID: 22859522, PMCID: PMC5450991, DOI: 10.1164/rccm.201202-0302oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBleomycinCells, CulturedCyclooxygenase 2Epithelial CellsGene Expression Regulation, EnzymologicHumansIdiopathic Pulmonary FibrosisLaser Capture MicrodissectionMatrix Metalloproteinases, SecretedMiceMice, KnockoutOligonucleotide Array Sequence AnalysisPulmonary AlveoliUp-RegulationConceptsIdiopathic pulmonary fibrosisHyperplastic epithelial cellsAlveolar epithelial cellsEpithelial cellsMMP-19IPF lungsWT miceLung fibrosisFibrotic responseHyperplastic alveolar epithelial cellsNovel mediatorLaser capture microscopeLung fibrotic responseDevelopment of fibrosisWild-type miceEpithelial phenotypic changesMatrix metalloproteinase-19Microarray analysisA549 epithelial cellsLung injuryBronchoalveolar lavagePulmonary fibrosisLung tissueSame lungFibrosisIntegrative Assessment of Chlorine-Induced Acute Lung Injury in Mice
Leikauf GD, Pope-Varsalona H, Concel VJ, Liu P, Bein K, Berndt A, Martin TM, Ganguly K, Jang AS, Brant KA, Dopico RA, Upadhyay S, Di YP, Li Q, Hu Z, Vuga LJ, Medvedovic M, Kaminski N, You M, Alexander DC, McDunn JE, Prows DR, Knoell DL, Fabisiak JP. Integrative Assessment of Chlorine-Induced Acute Lung Injury in Mice. American Journal Of Respiratory Cell And Molecular Biology 2012, 47: 234-244. PMID: 22447970, PMCID: PMC3423464, DOI: 10.1165/rcmb.2012-0026oc.Peer-Reviewed Original ResearchConceptsCandidate genesGenetic basisProtein catabolic processAcute lung injuryLung injuryHaplotype association mappingC57BLKS/JSingle nucleotide polymorphism associationsAssociation mappingMetabolomic profilingProtein transportCatabolic processTranscript levelsHaplotype mappingChromosome 1Chlorine-induced acute lung injuryAmino acid carrierSNP associationsReal-time PCRGenesGenetic associationMean survival timeRecognition sitesProfilingPromoter SNPs
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 hazardsHaplotype Association Mapping of Acute Lung Injury in Mice Implicates Activin A Receptor, Type 1
Leikauf GD, Concel VJ, Liu P, Bein K, Berndt A, Ganguly K, Jang AS, Brant KA, Dietsch M, Pope-Varsalona H, Dopico RA, Di YP, Li Q, Vuga LJ, Medvedovic M, Kaminski N, You M, Prows DR. Haplotype Association Mapping of Acute Lung Injury in Mice Implicates Activin A Receptor, Type 1. American Journal Of Respiratory And Critical Care Medicine 2011, 183: 1499-1509. PMID: 21297076, PMCID: PMC3137140, DOI: 10.1164/rccm.201006-0912oc.Peer-Reviewed Original ResearchConceptsDNA-protein bindingHaplotype association mappingSingle nucleotide polymorphism associationsAssociation mappingSNP associationsGenome-wide strategiesPrevious genetic analysisAcute lung injuryAmino acid substitutionsGenomic approachesLung injuryTranscription factorsCell signalingEnriched pathwaysCandidate genesSequence differencesChromosome 1Genetic analysisAssociated variantsAcid substitutionsActivin A receptorsGenesFunctional consequencesPolymorphism associationPolar strains