2021
Elevated 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
Genome-Wide Association Study of Susceptibility to Idiopathic Pulmonary Fibrosis
Allen RJ, Guillen-Guio B, Oldham JM, Ma SF, Dressen A, Paynton ML, Kraven LM, Obeidat M, Li X, Ng M, Braybrooke R, Molina-Molina M, Hobbs BD, Putman RK, Sakornsakolpat P, Booth HL, Fahy WA, Hart SP, Hill MR, Hirani N, Hubbard RB, McAnulty RJ, Millar AB, Navaratnam V, Oballa E, Parfrey H, Saini G, Whyte MKB, Zhang Y, Kaminski N, Adegunsoye A, Strek ME, Neighbors M, Sheng XR, Gudmundsson G, Gudnason V, Hatabu H, Lederer DJ, Manichaikul A, Newell JD, O’Connor G, Ortega VE, Xu H, Fingerlin TE, Bossé Y, Hao K, Joubert P, Nickle DC, Sin DD, Timens W, Furniss D, Morris AP, Zondervan KT, Hall IP, Sayers I, Tobin MD, Maher TM, Cho MH, Hunninghake GM, Schwartz DA, Yaspan BL, Molyneaux PL, Flores C, Noth I, Jenkins RG, Wain LV. Genome-Wide Association Study of Susceptibility to Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2020, 201: 564-574. PMID: 31710517, PMCID: PMC7047454, DOI: 10.1164/rccm.201905-1017oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedCase-Control StudiesCell Cycle ProteinsFemaleGene ExpressionGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansIdiopathic Pulmonary FibrosisIntracellular Signaling Peptides and ProteinsKinesinsMaleMiddle AgedRisk AssessmentSignal TransductionSpindle ApparatusTOR Serine-Threonine KinasesConceptsGenome-wide association studiesAssociation studiesIPF susceptibilityNew genome-wide significant signalsGenome-wide significant signalsGenome-wide analysisCell-cell adhesionLarge genome-wide association studiesImportance of mTORPolygenic risk score analysisTelomere maintenanceCausal genesFunctional analysisSusceptibility variantsRisk score analysisMultiple pathwaysGenetic associationGenesHost defensePolygenic risk scoresIndependent studiesPossible roleExpression associatesSignificant signalRecent studies
2019
BAL Cell Gene Expression in Severe Asthma Reveals Mechanisms of Severe Disease and Influences of Medications
Weathington N, O’Brien M, Radder J, Whisenant TC, Bleecker ER, Busse WW, Erzurum SC, Gaston B, Hastie A, Jarjour N, Meyers D, Milosevic J, Moore W, Tedrow J, Trudeau J, Wong H, Wu W, Kaminski N, Wenzel S, Modena B. BAL Cell Gene Expression in Severe Asthma Reveals Mechanisms of Severe Disease and Influences of Medications. American Journal Of Respiratory And Critical Care Medicine 2019, 200: 837-856. PMID: 31161938, PMCID: PMC6812436, DOI: 10.1164/rccm.201811-2221oc.Peer-Reviewed Original ResearchMeSH KeywordsAdrenergic beta-AgonistsAdultAsthmaBronchoalveolar Lavage FluidCase-Control StudiesCyclic AMPEosinophilsEpithelial CellsFemaleGene ExpressionHumansIn Vitro TechniquesLymphocytesMacrophages, AlveolarMaleNeutrophilsSequence Analysis, RNASeverity of Illness IndexSignal TransductionTHP-1 CellsConceptsCell gene expressionGene expressionAirway epithelial cell gene expressionEpithelial cell gene expressionGlobal gene expressionCellular gene expressionCell expression profilesAsthma susceptibility lociProtein levelsSystem-wide analysisExpression networksImportant disease mechanismCoexpression networkCellular milieuExpression changesExpression profilesSusceptibility lociCellular modelDisease mechanismsBiomolecular mechanismsNew targetsRobust upregulationSample traitsGenesExpressionBAL Cell Gene Expression Is Indicative of Outcome and Airway Basal Cell Involvement in Idiopathic Pulmonary Fibrosis
Prasse A, Binder H, Schupp JC, Kayser G, Bargagli E, Jaeger B, Hess M, Rittinghausen S, Vuga L, Lynn H, Violette S, Jung B, Quast K, Vanaudenaerde B, Xu Y, Hohlfeld JM, Krug N, Herazo-Maya JD, Rottoli P, Wuyts WA, Kaminski N. BAL Cell Gene Expression Is Indicative of Outcome and Airway Basal Cell Involvement in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2019, 199: 622-630. PMID: 30141961, PMCID: PMC6396865, DOI: 10.1164/rccm.201712-2551oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisAirway basal cellsChronic obstructive pulmonary diseaseObstructive pulmonary diseasePulmonary diseaseBAL cellsBasal cellsPulmonary fibrosisControl subjectsCell gene expressionIndependent IPF cohortsNine-gene signatureIPF cohortDerivation cohortClinical parametersRetrospective studyUnivariate analysisUnpredictable courseCell involvementDiscovery cohortGene expressionHealthy volunteersCox modelStage IIIFatal disease
2017
A Dirichlet process mixture model for clustering longitudinal gene expression data
Sun J, Herazo‐Maya J, Kaminski N, Zhao H, Warren JL. A Dirichlet process mixture model for clustering longitudinal gene expression data. Statistics In Medicine 2017, 36: 3495-3506. PMID: 28620908, PMCID: PMC5583037, DOI: 10.1002/sim.7374.Peer-Reviewed Original ResearchConceptsLongitudinal gene expression profilesDirichlet process prior distributionRegression coefficientsExtensive simulation studyLongitudinal gene expression dataBayesian settingPrior distributionClustering methodFactor analysis modelDimensionality challengeStatistical methodsSimulation studyNovel clustering methodHigh dimensionality challengeSubgroup identificationImportant problemGene expression dataInteresting subgroupsClusteringCoefficientAnalysis modelModelExpression dataMicrobes Are Associated with Host Innate Immune Response in Idiopathic Pulmonary Fibrosis
Huang Y, Ma SF, Espindola MS, Vij R, Oldham JM, Huffnagle GB, Erb-Downward JR, Flaherty KR, Moore BB, White ES, Zhou T, Li J, Lussier YA, Han MK, Kaminski N, Garcia JG, Hogaboam CM, Martinez FJ, Noth I. Microbes Are Associated with Host Innate Immune Response in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2017, 196: 208-219. PMID: 28157391, PMCID: PMC5519968, DOI: 10.1164/rccm.201607-1525oc.Peer-Reviewed Original ResearchConceptsProgression-free survivalMicrobial diversityRegulated signaling pathwaysNOD-like receptor signalingRNA sequencing dataGene expression dataMicroarray gene expression dataImmune response pathwaysMicrobial interactionsMicrobial communitiesHost innate immune responseResponse pathwaysLung microbial communityLeukocyte phenotypeImmune responseSequencing dataNetwork analysisShannon indexSignaling pathwaysToll-like receptor 9 stimulationExpression associationsExpression dataIndividual generaIdiopathic pulmonary fibrosis progressionOligomerization domain
2016
Gene Expression Correlated with Severe Asthma Characteristics Reveals Heterogeneous Mechanisms of Severe Disease
Modena BD, Bleecker ER, Busse WW, Erzurum SC, Gaston BM, Jarjour NN, Meyers DA, Milosevic J, Tedrow JR, Wu W, Kaminski N, Wenzel SE. Gene Expression Correlated with Severe Asthma Characteristics Reveals Heterogeneous Mechanisms of Severe Disease. American Journal Of Respiratory And Critical Care Medicine 2016, 195: 1449-1463. PMID: 27984699, PMCID: PMC5470748, DOI: 10.1164/rccm.201607-1407oc.Peer-Reviewed Original ResearchConceptsWeighted gene coexpression network analysisGene coexpression network analysisCoexpression network analysisGene expressionBiological processesAirway epithelial cell gene expressionEpithelial cell gene expressionNetwork of genesGene expression networksGene network modulesAsthma susceptibility lociT2 gene expressionCell gene expressionGene expression studiesNeuronal functionEpithelial growthMultiple molecular mechanismsExpression networksT2 genesGene networksUnderlying biological processesHub genesExpression studiesBiological insightsNetwork analysisExpression of RXFP1 Is Decreased in Idiopathic Pulmonary Fibrosis. Implications for Relaxin-based Therapies
Tan J, Tedrow JR, Dutta JA, Juan-Guardela B, Nouraie M, Chu Y, Trejo Bittar H, Ramani K, Biswas PS, Veraldi KL, Kaminski N, Zhang Y, Kass DJ. Expression of RXFP1 Is Decreased in Idiopathic Pulmonary Fibrosis. Implications for Relaxin-based Therapies. American Journal Of Respiratory And Critical Care Medicine 2016, 194: 1392-1402. PMID: 27310652, PMCID: PMC5148141, DOI: 10.1164/rccm.201509-1865oc.Peer-Reviewed Original ResearchConceptsRelaxin/insulin-like family peptide receptor 1Idiopathic pulmonary fibrosisIPF lung fibroblastsRXFP1 expressionLung fibroblastsPulmonary fibrosisFamily peptide receptor 1RXFP1 gene expressionLung Tissue Research ConsortiumPulmonary functionIPF lungsBleomycin injuryPotential therapyCollagen depositionFibrotic diseasesPatientsDemographic dataPotential efficacyReceptor 1Donor controlsTherapyRelaxin-like peptideGrowth factorGene expressionFibrosis
2015
A Novel Genomic Signature with Translational Significance for Human Idiopathic Pulmonary Fibrosis
Bauer Y, Tedrow J, de Bernard S, Birker-Robaczewska M, Gibson KF, Guardela BJ, Hess P, Klenk A, Lindell KO, Poirey S, Renault B, Rey M, Weber E, Nayler O, Kaminski N. A Novel Genomic Signature with Translational Significance for Human Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2015, 52: 217-231. PMID: 25029475, PMCID: PMC4370242, DOI: 10.1165/rcmb.2013-0310oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisHuman idiopathic pulmonary fibrosisLung fibrosis modelGrowth factor-β1IPF lungsPulmonary fibrosisFibrosis modelFactor-β1Therapeutic interventionsDevastating lung diseasePrimary human lung fibroblastsLung Tissue Research ConsortiumGene marker setsPotential therapeutic interventionsHuman lung fibroblastsEpithelial A549 cellsHuman epithelial A549 cellsBleomycin instillationLung fibrosisControl lungsLung diseaseControl cohortControl subjectsTranslational significanceNovel treatments
2014
Gene Expression in Relation to Exhaled Nitric Oxide Identifies Novel Asthma Phenotypes with Unique Biomolecular Pathways
Modena BD, Tedrow JR, Milosevic J, Bleecker ER, Meyers DA, Wu W, Bar-Joseph Z, Erzurum SC, Gaston BM, Busse WW, Jarjour NN, Kaminski N, Wenzel SE. Gene Expression in Relation to Exhaled Nitric Oxide Identifies Novel Asthma Phenotypes with Unique Biomolecular Pathways. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 1363-1372. PMID: 25338189, PMCID: PMC4294630, DOI: 10.1164/rccm.201406-1099oc.Peer-Reviewed Original ResearchConceptsEpithelial cell gene expressionCell gene expressionGene expressionAirway epithelial cell gene expressionGene expression patternsSevere Asthma Research ProgramActin cytoskeletonGene clusterGenomic studiesGene transcriptionGene pathwaysMolecular basisExpression patternsAsthma phenotypesWnt pathwayMicroarray platformGenesNovel pathwayPhenotypeBiomolecular pathwaysNeuronal functionPathwayUnadjusted p-valuesExpressionBiological characteristicsRelationship of DNA Methylation and Gene Expression in Idiopathic Pulmonary Fibrosis
Yang IV, Pedersen BS, Rabinovich E, Hennessy CE, Davidson EJ, Murphy E, Guardela BJ, Tedrow JR, Zhang Y, Singh MK, Correll M, Schwarz MI, Geraci M, Sciurba FC, Quackenbush J, Spira A, Kaminski N, Schwartz DA. Relationship of DNA Methylation and Gene Expression in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 1263-1272. PMID: 25333685, PMCID: PMC4315819, DOI: 10.1164/rccm.201408-1452oc.Peer-Reviewed Original ResearchConceptsGene expressionDNA methylationMethylation marksMethylation changesQuantitative trait lociTrans-gene expressionIntegrative genomic analysisTrait lociEpigenetic mechanismsTranscriptional changesGenomic analysisTranscription factorsCASZ1 expressionTarget genesFunctional validationExpression relationshipsMethylationGenesDMRsExpressionEnvironmental factorsTargeted analysisPathogenesis of IPFComplex interactionsTranscriptomeT-RECS: STABLE SELECTION OF DYNAMICALLY FORMED GROUPS OF FEATURES WITH APPLICATION TO PREDICTION OF CLINICAL OUTCOMES
Altman R, Dunker A, Hunter L, Ritchie M, Murray T, Klein T, HUANG G, TSAMARDINOS I, RAGHU V, KAMINSKI N, BENOS P. T-RECS: STABLE SELECTION OF DYNAMICALLY FORMED GROUPS OF FEATURES WITH APPLICATION TO PREDICTION OF CLINICAL OUTCOMES. Biocomputing 2014, 20: 431-42. PMID: 25592602, PMCID: PMC4299881, DOI: 10.1142/9789814644730_0041.Peer-Reviewed Original ResearchConceptsTraditional feature selection methodsFeature selection methodCohort of patientsPersonalized medicine strategiesReal expression dataFeature selectionClassification accuracyCluster selectionBiological datasetsClinical outcomesCluster featuresLung diseaseBreast cancerSelection methodPatient classificationStructured natureMedicine strategiesSurvival dataTarget variablesEfficient selectionCohortStable selectionImportant features
2013
Functional Genomic Assessment of Phosgene-Induced Acute Lung Injury in Mice
Leikauf GD, Concel VJ, Bein K, Liu P, Berndt A, Martin TM, Ganguly K, Jang AS, Brant KA, Dopico RA, Upadhyay S, Cario C, Di YP, Vuga LJ, Kostem E, Eskin E, You M, Kaminski N, Prows DR, Knoell DL, Fabisiak JP. Functional Genomic Assessment of Phosgene-Induced Acute Lung Injury in Mice. American Journal Of Respiratory Cell And Molecular Biology 2013, 49: 130522202035005. PMID: 23590305, PMCID: PMC3824050, DOI: 10.1165/rcmb.2012-0337oc.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAllelesAnimalsChemical Warfare AgentsChromosome MappingElectrophoretic Mobility Shift AssayFemaleGene ExpressionGene Expression ProfilingGenomeGenome-Wide Association StudyGenomicsGenotypeIntegrinsLungMiceMice, Inbred StrainsOligonucleotide Array Sequence AnalysisPhosgenePolymorphism, Single NucleotidePromoter Regions, GeneticReelin ProteinSodium-Potassium-Exchanging ATPaseConceptsSignificant SNP associationsSNP associationsTranscriptomic analysisCompetitive electrophoretic mobility shift analysisGenome-wide association mappingFunctional genomic assessmentPutative transcription factorElectrophoretic mobility shift analysisMobility shift analysisAssociation mappingGenetic resolutionTranscription factorsCandidate genesFunctional domainsNonsynonymous SNPsGenomic assessmentPhenotypic differencesPhenotypic extremesDiverse panelGenesGenetic determinantsShift analysisPTPRTAllelesITGA9Genome-wide association study identifies multiple susceptibility loci for pulmonary fibrosis
Fingerlin TE, Murphy E, Zhang W, Peljto AL, Brown KK, Steele MP, Loyd JE, Cosgrove GP, Lynch D, Groshong S, Collard HR, Wolters PJ, Bradford WZ, Kossen K, Seiwert SD, du Bois RM, Garcia CK, Devine MS, Gudmundsson G, Isaksson HJ, Kaminski N, Zhang Y, Gibson KF, Lancaster LH, Cogan JD, Mason WR, Maher TM, Molyneaux PL, Wells AU, Moffatt MF, Selman M, Pardo A, Kim DS, Crapo JD, Make BJ, Regan EA, Walek DS, Daniel JJ, Kamatani Y, Zelenika D, Smith K, McKean D, Pedersen BS, Talbert J, Kidd RN, Markin CR, Beckman KB, Lathrop M, Schwarz MI, Schwartz DA. Genome-wide association study identifies multiple susceptibility loci for pulmonary fibrosis. Nature Genetics 2013, 45: 613-620. PMID: 23583980, PMCID: PMC3677861, DOI: 10.1038/ng.2609.Peer-Reviewed Original ResearchmiR-199a-5p Is Upregulated during Fibrogenic Response to Tissue Injury and Mediates TGFbeta-Induced Lung Fibroblast Activation by Targeting Caveolin-1
Cardenas C, Henaoui IS, Courcot E, Roderburg C, Cauffiez C, Aubert S, Copin MC, Wallaert B, Glowacki F, Dewaeles E, Milosevic J, Maurizio J, Tedrow J, Marcet B, Lo-Guidice JM, Kaminski N, Barbry P, Luedde T, Perrais M, Mari B, Pottier N. miR-199a-5p Is Upregulated during Fibrogenic Response to Tissue Injury and Mediates TGFbeta-Induced Lung Fibroblast Activation by Targeting Caveolin-1. PLOS Genetics 2013, 9: e1003291. PMID: 23459460, PMCID: PMC3573122, DOI: 10.1371/journal.pgen.1003291.Peer-Reviewed Original ResearchConceptsIdiopathic formMiR-199aIPF patientsMouse modelUnilateral ureteral obstruction (UUO) mouse modelLung fibroblastsFibrotic lung diseaseLung fibroblast activationBile duct ligationPoor response ratesNew therapeutic strategiesCultured lung fibroblastsDifferent mouse strainsKey cell typesPulmonary expressionHistologic featuresPulmonary fibrosisFibroblastic fociLung diseaseLung fibrosisCurrent therapiesFibrogenic responseKidney fibrosisLiver fibrosisBleomycin exposure
2012
The isolation and characterization of renal cancer initiating cells from human Wilms' tumour xenografts unveils new therapeutic targets†
Pode‐Shakked N, Shukrun R, Mark‐Danieli M, Tsvetkov P, Bahar S, Pri‐Chen S, Goldstein RS, Rom‐Gross E, Mor Y, Fridman E, Meir K, Simon A, Magister M, Kaminski N, Goldmacher VS, Harari‐Steinberg O, Dekel B. The isolation and characterization of renal cancer initiating cells from human Wilms' tumour xenografts unveils new therapeutic targets†. EMBO Molecular Medicine 2012, 5: 18-37. PMID: 23239665, PMCID: PMC3569651, DOI: 10.1002/emmm.201201516.Peer-Reviewed Original ResearchMeSH KeywordsAC133 AntigenAldehyde DehydrogenaseAldehyde Dehydrogenase 1 FamilyAnimalsAntibodies, MonoclonalAntigens, CDCD56 AntigenCell DifferentiationCell ProliferationCell SeparationGene ExpressionGlycoproteinsHumansKidney NeoplasmsMaytansineMiceMice, Inbred NODMice, SCIDNeoplastic Stem CellsPeptidesRetinal DehydrogenaseTumor Cells, CulturedTumor Stem Cell AssayWilms TumorXenograft Model Antitumor AssaysConceptsNew therapeutic targetsTherapeutic targetPediatric solid tumorsPoor patient prognosisCancer initiating cellsMultiple xenograft modelsHuman WilmsCancer stem cellsAldehyde dehydrogenase activityMiR-200 familyPrimary tumorPatient prognosisRenal malignancyImmunodeficient micePediatric cancerXenograft modelTumor xenograftsXenograft cellsSolid tumorsTumor biologyComplete eradicationPediatric renal malignancyInitiating cellsProtein expressionTumorsProfibrotic Role of miR-154 in Pulmonary Fibrosis
Milosevic J, Pandit K, Magister M, Rabinovich E, Ellwanger DC, Yu G, Vuga LJ, Weksler B, Benos PV, Gibson KF, McMillan M, Kahn M, Kaminski N. Profibrotic Role of miR-154 in Pulmonary Fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2012, 47: 879-887. PMID: 23043088, PMCID: PMC3547095, DOI: 10.1165/rcmb.2011-0377oc.Peer-Reviewed Original ResearchMeSH KeywordsCase-Control StudiesCell MovementCell ProliferationCells, CulturedChromosomes, Human, Pair 14Cyclin-Dependent Kinase Inhibitor p15FibroblastsGene ExpressionHumansLungMicroRNAsMultigene FamilyOligonucleotide Array Sequence AnalysisPulmonary FibrosisRNA InterferenceTranscriptomeTransforming Growth Factor beta1Wnt Signaling PathwayConceptsIdiopathic pulmonary fibrosisNormal human lung fibroblastsMiR-154IPF lungsPulmonary fibrosisIPF fibroblastsProgressive interstitial lung diseaseInterstitial lung diseaseWnt/β-catenin pathwayHuman lung fibroblastsΒ-catenin pathwayTGF-β1 stimulationBinding of Smad3Quantitative RT-PCRLung diseaseProfibrotic roleExpression of microRNAsICG-001MiR-134Unknown originMiR-382MiR-487bProliferative effectLung fibroblastsMiR-410First-in-Human Trial of a STAT3 Decoy Oligonucleotide in Head and Neck Tumors: Implications for Cancer Therapy
Sen M, Thomas SM, Kim S, Yeh JI, Ferris RL, Johnson JT, Duvvuri U, Lee J, Sahu N, Joyce S, Freilino ML, Shi H, Li C, Ly D, Rapireddy S, Etter JP, Li PK, Wang L, Chiosea S, Seethala RR, Gooding WE, Chen X, Kaminski N, Pandit K, Johnson DE, Grandis JR. First-in-Human Trial of a STAT3 Decoy Oligonucleotide in Head and Neck Tumors: Implications for Cancer Therapy. Cancer Discovery 2012, 2: 694-705. PMID: 22719020, PMCID: PMC3668699, DOI: 10.1158/2159-8290.cd-12-0191.Peer-Reviewed Original ResearchConceptsSTAT3 target genesTarget genesSTAT3 target gene expressionSTAT3-selective inhibitorsTarget gene expressionInhibited xenograft growthSelective STAT3 inhibitorSystemic administrationTranscription factor decoyTranscription factorsSTAT3 proteinBroader clinical developmentGene expressionPhase 0 trialsSTAT3 inhibitorHuman cancersSTAT3Expression levelsSTAT3 decoyCancer cellsCellular viabilityNeck cancerSaline controlsNeck tumorsHuman trialsGlobal Methylation Patterns in Idiopathic Pulmonary Fibrosis
Rabinovich EI, Kapetanaki MG, Steinfeld I, Gibson KF, Pandit KV, Yu G, Yakhini Z, Kaminski N. Global Methylation Patterns in Idiopathic Pulmonary Fibrosis. PLOS ONE 2012, 7: e33770. PMID: 22506007, PMCID: PMC3323629, DOI: 10.1371/journal.pone.0033770.Peer-Reviewed Original ResearchConceptsCpG islandsMethylation patternsEpigenetic changesMethylation profilesHuman CpG island microarrayNuclear element-1 (LINE-1 or L1) retrotransposonsCellular biosynthetic processesCpG island microarrayGlobal methylation profilesRegulation of apoptosisGlobal methylation patternsLung phenotypeBRB-Array ToolsElement-1 (LINE-1 or L1) retrotransposonsCancer-specific changesBiosynthetic processesGlobal hypomethylationSpecific changesExtensive remodelingFalse discovery rateExtracellular matrix depositionArray resultsGenesHypomethylationLung cancer samples
2011
MicroRNAs in idiopathic pulmonary fibrosis
Pandit KV, Milosevic J, Kaminski N. MicroRNAs in idiopathic pulmonary fibrosis. Translational Research 2011, 157: 191-199. PMID: 21420029, DOI: 10.1016/j.trsl.2011.01.012.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisIPF lungsPulmonary fibrosisLung fibrosisMiR-155Vascular endothelial growth factor (VEGF) pathwayEndothelial growth factor pathwayLethal fibrotic lung diseaseFibrotic lung diseaseMiR-29Upregulated miR-155Growth factor-β1Epithelial-mesenchymal transitionGrowth factor pathwaysLung epithelial cellsLung diseaseProfibrotic effectsBleomycin modelRole of microRNAsTherapeutic targetFactor-β1FibrosisMesenchymal transitionFactor pathwayLet-7 family members