2023
Somatic Mutations: The Next Frontier in Demystifying Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis?
Yan X, Kaminski N. Somatic Mutations: The Next Frontier in Demystifying Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis? American Journal Of Respiratory And Critical Care Medicine 2023, 208: 1150-1151. PMID: 37856835, PMCID: PMC10868359, DOI: 10.1164/rccm.202310-1774ed.Peer-Reviewed Original ResearchMeSH KeywordsHumansIdiopathic Pulmonary FibrosisLungLung DiseasesMutationPulmonary Disease, Chronic ObstructiveIntegrative genetic and genomic networks identify microRNA associated with COPD and ILD
Pavel A, Garrison C, Luo L, Liu G, Taub D, Xiao J, Juan-Guardela B, Tedrow J, Alekseyev Y, Yang I, Geraci M, Sciurba F, Schwartz D, Kaminski N, Beane J, Spira A, Lenburg M, Campbell J. Integrative genetic and genomic networks identify microRNA associated with COPD and ILD. Scientific Reports 2023, 13: 13076. PMID: 37567908, PMCID: PMC10421936, DOI: 10.1038/s41598-023-39751-w.Peer-Reviewed Original ResearchMeSH KeywordsGenomicsHumansLungLung Diseases, InterstitialMicroRNAsPulmonary Disease, Chronic ObstructiveConceptsSeed sequenceGene expressionShort RNA sequencingAirway differentiationIntegrative network analysisExpression networksRNA sequencingGenomic networksMiRNA regulatorsMiRNA isoformsNotch pathwayIsomiRsDistinct subclustersSNP microarraysGenesMicroRNAsMolecular heterogeneityILD pathogenesisDisease networkOverexpressionSequenceExpressionNetwork analysisDifferentiationGrb2A statistical framework to identify cell types whose genetically regulated proportions are associated with complex diseases
Liu W, Deng W, Chen M, Dong Z, Zhu B, Yu Z, Tang D, Sauler M, Lin C, Wain L, Cho M, Kaminski N, Zhao H. A statistical framework to identify cell types whose genetically regulated proportions are associated with complex diseases. PLOS Genetics 2023, 19: e1010825. PMID: 37523391, PMCID: PMC10414598, DOI: 10.1371/journal.pgen.1010825.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsFemaleGene Expression ProfilingGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLungPolymorphism, Single NucleotidePulmonary Disease, Chronic ObstructiveConceptsCell typesDisease-associated tissuesWide association studyComplex diseasesCell type proportionsDisease-relevant tissuesReal GWAS dataFunctional genesTranscriptomic dataGWAS dataGenetic dataAssociation studiesNovel statistical frameworkChronic obstructive pulmonary diseaseStatistical frameworkObstructive pulmonary diseaseIdiopathic pulmonary fibrosisBreast cancer riskType proportionsBlood CD8Pulmonary diseasePulmonary fibrosisPredictive biomarkersLung tissueBreast cancer
2022
Characterization of the COPD alveolar niche using single-cell RNA sequencing
Sauler M, McDonough JE, Adams TS, Kothapalli N, Barnthaler T, Werder RB, Schupp JC, Nouws J, Robertson MJ, Coarfa C, Yang T, Chioccioli M, Omote N, Cosme C, Poli S, Ayaub EA, Chu SG, Jensen KH, Gomez JL, Britto CJ, Raredon MSB, Niklason LE, Wilson AA, Timshel PN, Kaminski N, Rosas IO. Characterization of the COPD alveolar niche using single-cell RNA sequencing. Nature Communications 2022, 13: 494. PMID: 35078977, PMCID: PMC8789871, DOI: 10.1038/s41467-022-28062-9.Peer-Reviewed Original ResearchConceptsSingle-cell RNA sequencingRNA sequencingCell-specific mechanismsChronic obstructive pulmonary diseaseAdvanced chronic obstructive pulmonary diseaseTranscriptomic network analysisSingle-cell RNA sequencing profilesCellular stress toleranceAberrant cellular metabolismStress toleranceRNA sequencing profilesTranscriptional evidenceCellular metabolismAlveolar nicheSequencing profilesHuman alveolar epithelial cellsChemokine signalingAlveolar epithelial type II cellsObstructive pulmonary diseaseSitu hybridizationType II cellsEpithelial type II cellsSequencingCOPD pathobiologyHuman lung tissue samples
2021
MicroRNA miR-24-3p reduces DNA damage responses, apoptosis, and susceptibility to chronic obstructive pulmonary disease
Nouws J, Wan F, Finnemore E, Roque W, Kim SJ, Bazan IS, Li CX, Sköld C, Dai Q, Yan X, Chioccioli M, Neumeister V, Britto CJ, Sweasy J, Bindra RS, Wheelock ÅM, Gomez JL, Kaminski N, Lee PJ, Sauler M. MicroRNA miR-24-3p reduces DNA damage responses, apoptosis, and susceptibility to chronic obstructive pulmonary disease. JCI Insight 2021, 6: e134218. PMID: 33290275, PMCID: PMC7934877, DOI: 10.1172/jci.insight.134218.Peer-Reviewed Original ResearchConceptsCellular stress responseStress responseHomology-directed DNA repairDNA damage responseProtein BRCA1Damage responseCellular stressDNA repairProtein BimCOPD lung tissueLung epithelial cellsCellular responsesExpression arraysEpithelial cell apoptosisDNA damageChronic obstructive pulmonary diseaseBRCA1 expressionCell apoptosisApoptosisEpithelial cellsCritical mechanismMicroRNAsRegulatorObstructive pulmonary diseaseIncreases SusceptibilityElevated plasma level of Pentraxin 3 is associated with emphysema and mortality in smokers
Zhang Y, Tedrow J, Nouraie M, Li X, Chandra D, Bon J, Kass DJ, Fuhrman CR, Leader JK, Duncan SR, Kaminski N, Sciurba FC. Elevated plasma level of Pentraxin 3 is associated with emphysema and mortality in smokers. Thorax 2021, 76: 335-342. PMID: 33479043, PMCID: PMC8249179, DOI: 10.1136/thoraxjnl-2020-215356.Peer-Reviewed Original ResearchConceptsAirflow obstructionPlasma levelsLung tissueEmphysema severitySmoking-related lung diseaseAssociation of lungExpiratory airflow obstructionFormer tobacco smokersLevels of PTX3PTX3 gene expressionElevated plasma levelsHyaluronic acid levelsBlood of subjectsPlasma PTX3PTX3 levelsLung functionTobacco exposureClinical outcomesTobacco smokersLung diseasePentraxin 3Predictive biomarkersPTX3 expressionLower riskDisease patterns
2020
Gene coexpression networks reveal novel molecular endotypes in alpha-1 antitrypsin deficiency
Chu JH, Zang W, Vukmirovic M, Yan X, Adams T, DeIuliis G, Hu B, Mihaljinec A, Schupp JC, Becich MJ, Hochheiser H, Gibson KF, Chen ES, Morris A, Leader JK, Wisniewski SR, Zhang Y, Sciurba FC, Collman RG, Sandhaus R, Herzog EL, Patterson KC, Sauler M, Strange C, Kaminski N. Gene coexpression networks reveal novel molecular endotypes in alpha-1 antitrypsin deficiency. Thorax 2020, 76: 134-143. PMID: 33303696, PMCID: PMC10794043, DOI: 10.1136/thoraxjnl-2019-214301.Peer-Reviewed Original ResearchMeSH KeywordsAdultAlpha 1-Antitrypsin DeficiencyBronchoalveolar Lavage FluidFemaleGene Expression ProfilingGene Regulatory NetworksGenotypeHumansMaleMiddle AgedNeutrophilsProspective StudiesPulmonary Disease, Chronic ObstructiveTranscriptomeConceptsWeighted gene co-expression network analysisAlpha-1 antitrypsin deficiencyGene modulesGene co-expression network analysisDifferential gene expression analysisCo-expression network analysisPeripheral blood mononuclear cellsGene expression patternsPBMC gene expression patternsGene coexpression networksAATD individualsGene expression profilesGene expression analysisBronchoalveolar lavageAugmentation therapyClinical variablesAntitrypsin deficiencyGene expression assaysRNA-seqCoexpression networkGene validationExpression analysisExpression assaysWGCNA modulesExpression patternsSingle-cell RNA-seq reveals ectopic and aberrant lung-resident cell populations in idiopathic pulmonary fibrosis
Adams TS, Schupp JC, Poli S, Ayaub EA, Neumark N, Ahangari F, Chu SG, Raby BA, DeIuliis G, Januszyk M, Duan Q, Arnett HA, Siddiqui A, Washko GR, Homer R, Yan X, Rosas IO, Kaminski N. Single-cell RNA-seq reveals ectopic and aberrant lung-resident cell populations in idiopathic pulmonary fibrosis. Science Advances 2020, 6: eaba1983. PMID: 32832599, PMCID: PMC7439502, DOI: 10.1126/sciadv.aba1983.Peer-Reviewed Original ResearchMeSH KeywordsEndothelial CellsHumansIdiopathic Pulmonary FibrosisLungPulmonary Disease, Chronic ObstructiveRNA-SeqConceptsIdiopathic pulmonary fibrosisVascular endothelial cellsIPF lungsPulmonary fibrosisChronic obstructive pulmonary disease (COPD) lungsFatal interstitial lung diseaseEndothelial cellsInterstitial lung diseaseCell populationsIPF myofibroblastsMyofibroblast fociNonsmoker controlsLung diseaseCOPD lungsBasaloid cellsSingle-cell atlasInvasive fibroblastsMacrophage populationsLungStromal cellsEpithelial cellsFibrosisCellular populationsDevelopmental markersSingle-cell RNA-seq
2018
The DNA repair transcriptome in severe COPD
Sauler M, Lamontagne M, Finnemore E, Herazo-Maya JD, Tedrow J, Zhang X, Morneau JE, Sciurba F, Timens W, Paré PD, Lee PJ, Kaminski N, Bossé Y, Gomez JL. The DNA repair transcriptome in severe COPD. European Respiratory Journal 2018, 52: 1701994. PMID: 30190272, PMCID: PMC6422831, DOI: 10.1183/13993003.01994-2017.Peer-Reviewed Original ResearchMeSH KeywordsAgedDNA DamageDNA RepairFemaleGene Expression ProfilingHumansImmunohistochemistryLungMaleMiddle AgedPulmonary Disease, Chronic ObstructiveTranscriptomeConceptsDNA damage toleranceDNA repairInadequate DNA repairSevere chronic obstructive pulmonary diseaseChronic obstructive pulmonary diseaseRepair pathwaysGene correlation network analysisIntegrative genomics approachNucleotide excision repair pathwayDNA repair pathwaysGene Set Enrichment AnalysisExcision repair pathwayGlobal transcriptomic profilesDNA repair genesDNA repair responseCorrelation network analysisCOPD severityGenomic approachesLung tissue transcriptomeTranscriptomic differencesTranscriptomic changesTranscriptomic patternsRNA sequencingTissue transcriptomesTranscriptomic profilesHypercapnia increases airway smooth muscle contractility via caspase-7–mediated miR-133a–RhoA signaling
Shigemura M, Lecuona E, Angulo M, Homma T, Rodríguez DA, Gonzalez-Gonzalez FJ, Welch LC, Amarelle L, Kim SJ, Kaminski N, Budinger GRS, Solway J, Sznajder JI. Hypercapnia increases airway smooth muscle contractility via caspase-7–mediated miR-133a–RhoA signaling. Science Translational Medicine 2018, 10 PMID: 30185650, PMCID: PMC6889079, DOI: 10.1126/scitranslmed.aat1662.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAgedAged, 80 and overAirway ResistanceAnimalsCalciumCalpainCarbon DioxideCaspase 7Chronic DiseaseDown-RegulationEnzyme ActivationFemaleHumansHypercapniaMaleMEF2 Transcription FactorsMice, Inbred C57BLMicroRNAsMiddle AgedMuscle ContractionMuscle, SmoothMyocytes, Smooth MusclePulmonary Disease, Chronic ObstructiveRhoA GTP-Binding ProteinSignal TransductionConceptsChronic obstructive pulmonary diseaseAirway smooth muscle cellsSmooth muscle cellsMouse airway smooth muscle cellsSevere chronic obstructive pulmonary diseaseHuman airway smooth muscle cellsAirway smooth muscle contractilityMuscle cellsCorrection of hypercapniaSmooth muscle cell contractionCohort of patientsObstructive pulmonary diseaseHigh airway resistanceSevere lung diseaseDevelopment of hypercapniaSmooth muscle contractilityMuscle cell contractionRas homolog family member AMyosin light chain phosphorylationAirway contractilityAirway contractionHypercapnic patientsCOPD severityPulmonary diseaseAirway resistance
2017
Extreme Trait Whole-Genome Sequencing Identifies PTPRO as a Novel Candidate Gene in Emphysema with Severe Airflow Obstruction
Radder JE, Zhang Y, Gregory AD, Yu S, Kelly NJ, Leader JK, Kaminski N, Sciurba FC, Shapiro SD. Extreme Trait Whole-Genome Sequencing Identifies PTPRO as a Novel Candidate Gene in Emphysema with Severe Airflow Obstruction. American Journal Of Respiratory And Critical Care Medicine 2017, 196: 159-171. PMID: 28199135, PMCID: PMC5519967, DOI: 10.1164/rccm.201606-1147oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMaleMiddle AgedPulmonary Disease, Chronic ObstructivePulmonary EmphysemaReceptor-Like Protein Tyrosine Phosphatases, Class 3Severity of Illness IndexConceptsNovel candidate genesCandidate genesSuggestive associationSuggestive candidate genesRare genetic variationRare variationRegion-based testsGene-based testsSingle-variant testsRare nonsynonymous variantsWhole-genome sequencingRare variantsWhole genome sequencing resultsGenomic regionsGenetic variationGenetic association studiesDisease heritabilityCellular pathwaysAssociation studiesExtreme phenotypesPTPRONonsynonymous variantsSequencing resultsGenesDisease susceptibility
2016
Integrated Genomics Reveals Convergent Transcriptomic Networks Underlying Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis
Kusko RL, Brothers JF, Tedrow J, Pandit K, Huleihel L, Perdomo C, Liu G, Juan-Guardela B, Kass D, Zhang S, Lenburg M, Martinez F, Quackenbush J, Sciurba F, Limper A, Geraci M, Yang I, Schwartz DA, Beane J, Spira A, Kaminski N. Integrated Genomics Reveals Convergent Transcriptomic Networks Underlying Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2016, 194: 948-960. PMID: 27104832, PMCID: PMC5067817, DOI: 10.1164/rccm.201510-2026oc.Peer-Reviewed Original ResearchMeSH KeywordsAdultEmphysemaFemaleGene Regulatory NetworksHumansHypoxia-Inducible Factor 1, alpha SubunitIdiopathic Pulmonary FibrosisI-kappa B ProteinsMaleMembrane ProteinsMiddle AgedNerve Tissue ProteinsOligonucleotide Array Sequence AnalysisPlatelet-Derived Growth FactorProto-Oncogene Proteins c-mdm2Pulmonary Disease, Chronic ObstructiveConceptsChronic obstructive pulmonary diseaseIdiopathic pulmonary fibrosisObstructive pulmonary diseasePulmonary diseasePulmonary fibrosisNCounter Analysis SystemHypoxia pathwayQuantitative polymerase chain reactionTranscriptomic pathwaysPolymerase chain reactionIndependent cohortEmphysemaIndependent sample setDiseaseGene expression arraysEnvironmental exposuresChain reactionFibrosisLungMolecular mechanismsExpression arraysMiR96Integrative genomics approachTranscriptional regulatory hubsPathway
2015
Rationale and Design of the Genomic Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis Study. Alpha-1 Protocol
Strange C, Senior RM, Sciurba F, O’Neal S, Morris A, Wisniewski SR, Bowler R, Hochheiser HS, Becich MJ, Zhang Y, Leader JK, Methé BA, Kaminski N, Sandhaus RA, Group* F. Rationale and Design of the Genomic Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis Study. Alpha-1 Protocol. Annals Of The American Thoracic Society 2015, 12: 1551-1560. PMID: 26153726, PMCID: PMC4627425, DOI: 10.1513/annalsats.201503-143oc.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAlpha 1-Antitrypsin DeficiencyBronchoalveolar LavageCross-Sectional StudiesExercise ToleranceFemaleGenomicsGenotypeHumansMaleMicrobiotaMiddle AgedPhenotypeProspective StudiesPulmonary Disease, Chronic ObstructivePulmonary EmphysemaResearch DesignRespiratory Function TestsSarcoidosisTomography, X-Ray ComputedConceptsAlpha-1 antitrypsin deficiencyAugmentation therapyBronchoalveolar lavageAntitrypsin deficiencyClinical presentationPiZZ individualsAlpha-1-antitrypsin augmentation therapyAlpha-1 antitrypsin genotypeChronic obstructive pulmonary disease phenotypesPulmonary function testingAge 35 yearsVariable clinical presentationCross-sectional studyAlpha-1 antitrypsinIntermediate outcome measuresPulmonary disease phenotypesUnique genetic causeExercise capacityTherapeutic trialsChest tomographyClinical symptomsCOPD pathogenesisCOPD phenotypesFunction testingCOPD StudySuppression of NLRX1 in chronic obstructive pulmonary disease
Kang MJ, Yoon CM, Kim BH, Lee CM, Zhou Y, Sauler M, Homer R, Dhamija A, Boffa D, West AP, Shadel GS, Ting JP, Tedrow JR, Kaminski N, Kim WJ, Lee CG, Oh YM, Elias JA. Suppression of NLRX1 in chronic obstructive pulmonary disease. Journal Of Clinical Investigation 2015, 125: 2458-2462. PMID: 25938787, PMCID: PMC4497738, DOI: 10.1172/jci71747.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseObstructive pulmonary diseaseCigarette smokeAlveolar destructionPulmonary diseaseHuman chronic obstructive pulmonary diseaseExpression of NLRX1Innate immune pathwaysInnate immune responseQuality of lifeCOPD patientsPulmonary functionSubsequent inflammationImmune responseInflammasome activationMurine modelIndependent cohortImmune pathwaysInflammationDisease severityInflammasome responseImportant mediatorCell apoptosisNLRX1Tissue effects
2014
Secreted Phosphoprotein 1 Is a Determinant of Lung Function Development in Mice
Ganguly K, Martin TM, Concel VJ, Upadhyay S, Bein K, Brant KA, George L, Mitra A, Thimraj TA, Fabisiak JP, Vuga LJ, Fattman C, Kaminski N, Schulz H, Leikauf GD. Secreted Phosphoprotein 1 Is a Determinant of Lung Function Development in Mice. American Journal Of Respiratory Cell And Molecular Biology 2014, 51: 637-651. PMID: 24816281, PMCID: PMC4224082, DOI: 10.1165/rcmb.2013-0471oc.Peer-Reviewed Original ResearchMeSH KeywordsAlveolar Epithelial CellsAnimalsAnimals, NewbornCore Binding Factor Alpha 1 SubunitFemaleGene Expression Regulation, DevelopmentalLung ComplianceMaleMice, Inbred C3HMice, Inbred C57BLMice, KnockoutOligonucleotide Array Sequence AnalysisOsteopontinPromoter Regions, GeneticPulmonary AlveoliPulmonary Disease, Chronic ObstructiveReceptor, Notch1ConceptsMicroarray analysisPhosphoprotein 1Quantitative trait lociLung functionQuantitative RT-PCR analysisDNA-protein bindingRunt-related transcription factor 2Transcription factor 2Developmental transcriptsLung developmentTrait lociNumerous genesSecreted Phosphoprotein 1Notch1 transcriptsRT-PCR analysisInsulin-like growth factor-1C3H/HeJ miceDiminished lung functionLung function developmentSPP1 promoterSPP1Growth factor-1Mean airspace chord lengthC3H/HeJGenetic variantsC-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 emphysemaPneumocystis jirovecii colonization is associated with enhanced Th1 inflammatory gene expression in lungs of humans with chronic obstructive pulmonary disease
Fitzpatrick ME, Tedrow JR, Hillenbrand ME, Lucht L, Richards T, Norris KA, Zhang Y, Sciurba FC, Kaminski N, Morris A. Pneumocystis jirovecii colonization is associated with enhanced Th1 inflammatory gene expression in lungs of humans with chronic obstructive pulmonary disease. Microbiology And Immunology 2014, 58: 202-211. PMID: 24438206, PMCID: PMC4106795, DOI: 10.1111/1348-0421.12135.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedChemokines, CXCFemaleHumansLungMaleMiddle AgedPneumocystis cariniiPneumonia, PneumocystisPulmonary Disease, Chronic ObstructiveTh1 CellsUp-RegulationConceptsChronic obstructive pulmonary diseaseObstructive pulmonary diseaseLung Tissue Research ConsortiumPneumocystis colonizationPulmonary diseaseCOPD pathogenesisLung gene expression profilesChemokine ligands CXCL9Cognate receptor CXCR3Finding of upregulationLungs of humansInflammatory gene expressionLung tissue samplesPotential key pathwaysGene expression profilesPneumocystis jirovecii colonizationReceptor CXCR3Ligands CXCL9Lymphocyte traffickingT lymphocytesInflammatory genesPneumocystis jiroveciiDisease pathogenesisExpression profilesLigand expression
2013
Assessment of lung volume collapsibility in chronic obstructive lung disease patients using CT
Kundu S, Gu S, Leader JK, Tedrow JR, Sciurba FC, Gur D, Kaminski N, Pu J. Assessment of lung volume collapsibility in chronic obstructive lung disease patients using CT. European Radiology 2013, 23: 1564-1572. PMID: 23494492, PMCID: PMC3657332, DOI: 10.1007/s00330-012-2746-1.Peer-Reviewed Original ResearchMeSH KeywordsAgedAlgorithmsFemaleHumansLungMaleMiddle AgedPulmonary Disease, Chronic ObstructiveRadiographic Image Interpretation, Computer-AssistedRespiratory Function TestsTomography, X-Ray ComputedConceptsPulmonary function testsUpper lobeLower lobeWhole lungLung lobesChronic obstructive lung disease patientsDisease severityGOLD categoriesObstructive lung disease patientsLung disease patientsMean lung densityTotal lung volumeAssessment of lungLobar volume changesFEV1/Lung functionExpiration volumeFunction testsGOLD classificationInspiration/expirationDisease patientsRV/Air trappingLung volumeCT examinations
2012
Retinoic Acid–related Orphan Receptor-α Is Induced in the Setting of DNA Damage and Promotes Pulmonary Emphysema
Shi Y, Cao J, Gao J, Zheng L, Goodwin A, An CH, Patel A, Lee JS, Duncan SR, Kaminski N, Pandit KV, Rosas IO, Choi AM, Morse D. Retinoic Acid–related Orphan Receptor-α Is Induced in the Setting of DNA Damage and Promotes Pulmonary Emphysema. American Journal Of Respiratory And Critical Care Medicine 2012, 186: 412-419. PMID: 22744720, PMCID: PMC5450975, DOI: 10.1164/rccm.201111-2023oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersCells, CulturedDisease Models, AnimalDNA DamageDNA RepairGene Expression ProfilingHumansLungMiceMice, Inbred C57BLMice, Neurologic MutantsNuclear Receptor Subfamily 1, Group F, Member 1Oligonucleotide Array Sequence AnalysisPulmonary Disease, Chronic ObstructivePulmonary EmphysemaTobacco Smoke PollutionConceptsRetinoic acid-related orphan receptorAcid-related orphan receptorCigarette smoke extractLungs of patientsPathogenesis of emphysemaRORA expressionCigarette smokeAirspace enlargementSmoke extractCigarette smoke exposureSmoke-induced emphysemaOrphan receptorDNA damageActive smokingLung transplantationSmoke exposureLung cancerPulmonary emphysemaLung tissueEmphysemaPatientsGene expression profilingApoptotic cell deathMiceEnhanced susceptibility
2009
The Influence of Radiographic Phenotype and Smoking Status on Peripheral Blood Biomarker Patterns in Chronic Obstructive Pulmonary Disease
Bon JM, Leader JK, Weissfeld JL, Coxson HO, Zheng B, Branch RA, Kondragunta V, Lee JS, Zhang Y, Choi AM, Lokshin AE, Kaminski N, Gur D, Sciurba FC. The Influence of Radiographic Phenotype and Smoking Status on Peripheral Blood Biomarker Patterns in Chronic Obstructive Pulmonary Disease. PLOS ONE 2009, 4: e6865. PMID: 19718453, PMCID: PMC2730536, DOI: 10.1371/journal.pone.0006865.Peer-Reviewed Original ResearchMeSH KeywordsAgedBiomarkersCohort StudiesFemaleForced Expiratory VolumeHumansMaleMiddle AgedPulmonary Disease, Chronic ObstructiveSmokingTomography, X-Ray ComputedConceptsChronic obstructive pulmonary diseaseObstructive pulmonary diseaseCurrent smoking statusAirway thickeningSmoking statusPulmonary diseaseBiomarker patternsSerum biomarker patternsSerum biomarker profilesSerum inflammatory proteinsParenchymal phenotypesMeasurements of FEV1Cross-sectional studyMultiplex protein arrayUnique biomarker patternsQuantitative CT measurementsCOPD syndromePhysiologic obstructionSecond percentAirway remodelingExpiratory volumeInflammatory markersParenchymal destructionScreening cohortBiological therapy