2024
Noninvasive assessment of the lung inflammation-fibrosis axis by targeted imaging of CMKLR1
Mannes P, Adams T, Farsijani S, Barnes C, Latoche J, Day K, Nedrow J, Ahangari F, Kaminski N, Lee J, Tavakoli S. Noninvasive assessment of the lung inflammation-fibrosis axis by targeted imaging of CMKLR1. Science Advances 2024, 10: eadm9817. PMID: 38896611, PMCID: PMC11186491, DOI: 10.1126/sciadv.adm9817.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisFibrotic lung diseaseRisk stratificationMurine modelLung fibrosisLung diseaseModel of bleomycin-induced lung fibrosisBleomycin-induced lung fibrosisImaging biomarkersMurine model of bleomycin-induced lung fibrosisBronchoalveolar lavage cellsMonocyte-derived macrophagesPositron emission tomographyInflammatory endotypesPulmonary fibrosisLavage cellsPoor survivalNoninvasive assessmentTherapeutic monitoringEmission tomographyCMKLR1FibrosisClinical trajectoryLungLung regions
2019
Transcriptional regulatory model of fibrosis progression in the human lung
McDonough JE, Ahangari F, Li Q, Jain S, Verleden SE, Herazo-Maya J, Vukmirovic M, DeIuliis G, Tzouvelekis A, Tanabe N, Chu F, Yan X, Verschakelen J, Homer RJ, Manatakis DV, Zhang J, Ding J, Maes K, De Sadeleer L, Vos R, Neyrinck A, Benos PV, Bar-Joseph Z, Tantin D, Hogg JC, Vanaudenaerde BM, Wuyts WA, Kaminski N. Transcriptional regulatory model of fibrosis progression in the human lung. JCI Insight 2019, 4 PMID: 31600171, PMCID: PMC6948862, DOI: 10.1172/jci.insight.131597.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisAdvanced fibrosisAlveolar surface densityFibrosis progressionLung fibrosisHuman lungDynamic Regulatory Events MinerExtent of fibrosisIPF lungsPulmonary fibrosisControl lungsIPF tissueB lymphocytesFibrosisLungLinear mixed-effects modelsMixed-effects modelsGene expression changesSystems biology modelsDifferential gene expression analysisGene expression analysisProgressionGene expression networksRNA sequencingBiology modelsIntegrating multiomics longitudinal data to reconstruct networks underlying lung development
Ding J, Ahangari F, Espinoza CR, Chhabra D, Nicola T, Yan X, Lal CV, Hagood JS, Kaminski N, Bar-Joseph Z, Ambalavanan N. Integrating multiomics longitudinal data to reconstruct networks underlying lung development. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2019, 317: l556-l568. PMID: 31432713, PMCID: PMC6879899, DOI: 10.1152/ajplung.00554.2018.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornChildChild, PreschoolDNA MethylationEpigenesis, GeneticFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalGene Regulatory NetworksHigh-Throughput Nucleotide SequencingHumansImmunity, InnateInfantInfant, NewbornLungMaleMiceMice, Inbred C57BLMicroRNAsOrganogenesisProteomicsPulmonary AlveoliRNA, MessengerSingle-Cell AnalysisTranscriptomeConceptsSingle-cell RNA-seq dataLung developmentDynamic regulatory networksOmics data setsRNA-seq dataIndividual cell typesHuman lung developmentRegulatory networksDNA methylationLaser capture microdissectionEpigenetic changesExpression trajectoriesKey pathwaysCell typesActive pathwaysCapture microdissectionRegulatorKey eventsInnate immunityNew insightsSpecific key eventsPathwayComprehensive understandingProteomicsMethylation
2018
A role for telomere length and chromosomal damage in idiopathic pulmonary fibrosis
McDonough JE, Martens DS, Tanabe N, Ahangari F, Verleden SE, Maes K, Verleden GM, Kaminski N, Hogg JC, Nawrot TS, Wuyts WA, Vanaudenaerde BM. A role for telomere length and chromosomal damage in idiopathic pulmonary fibrosis. Respiratory Research 2018, 19: 132. PMID: 29986708, PMCID: PMC6038197, DOI: 10.1186/s12931-018-0838-4.Peer-Reviewed Original ResearchConceptsIPF lungsDisease severityChromosomal damagePulmonary fibrosisTelomere lengthBackgroundIdiopathic pulmonary fibrosisRegional disease severityStructural disease severityIdiopathic pulmonary fibrosisFatal lung diseaseAirway epithelial cellsMultivariate linear mixed-effects modelDonor lungsFibroblastic fociLung diseaseFibrotic markersTransplant surgeryPathological changesSevere diseaseLungLinear mixed-effects modelsQuantitative histologyMixed-effects modelsExtracellular matrixSeverity
2012
YKL-40, a Chitinase-like Protein at the Intersection of Inflammation and Remodeling
Lee CG, Dela Cruz CS, Herzog E, Rosenberg SM, Ahangari F, Elias JA. YKL-40, a Chitinase-like Protein at the Intersection of Inflammation and Remodeling. American Journal Of Respiratory And Critical Care Medicine 2012, 185: 692-694. PMID: 22467800, DOI: 10.1164/rccm.201202-0203ed.Books
2002
Mice heterozygous for mutation in Atm, the gene involved in ataxia-telangiectasia, have heightened susceptibility to cancer
Spring K, Ahangari F, Scott SP, Waring P, Purdie DM, Chen PC, Hourigan K, Ramsay J, McKinnon PJ, Swift M, Lavin MF. Mice heterozygous for mutation in Atm, the gene involved in ataxia-telangiectasia, have heightened susceptibility to cancer. Nature Genetics 2002, 32: 185-190. PMID: 12195425, DOI: 10.1038/ng958.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell SurvivalChromosomesDNA-Binding ProteinsFemaleGamma RaysGenetic Predisposition to DiseaseHeterozygoteHumansMaleMiceMice, Inbred C57BLMutation, MissenseNeoplasmsPenetranceProtein Serine-Threonine KinasesTumor Suppressor ProteinsConceptsAtaxia telangiectasiaATM kinase activityDominant negative effectATM cDNAGenome instabilityHeterozygous miceRadiation-induced chromosomal aberrationsKinase activityCancer predispositionFrame deletionMutationsControl cellsGenesChromosomal aberrationsCellsCDNAMouse carriersDeletionMiceHeterozygous carriersAtmFirst timeExpressionFurther support
2001
Atm knock-in mice harboring an in-frame deletion corresponding to the human ATM 7636del9 common mutation exhibit a variant phenotype.
Spring K, Cross S, Li C, Watters D, Ben-Senior L, Waring P, Ahangari F, Lu SL, Chen P, Misko I, Paterson C, Kay G, Smorodinsky NI, Shiloh Y, Lavin MF. Atm knock-in mice harboring an in-frame deletion corresponding to the human ATM 7636del9 common mutation exhibit a variant phenotype. Cancer Research 2001, 61: 4561-8. PMID: 11389091.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsBase SequenceCell Cycle ProteinsCrosses, GeneticDNADNA-Binding ProteinsFemaleHumansLymphomaMaleMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsMutagenesis, Site-DirectedPhenotypeProtein Serine-Threonine KinasesSequence DeletionThymus NeoplasmsTumor Suppressor ProteinsUp-RegulationConceptsAtaxia telangiectasiaFrame deletionDisorder ataxia-telangiectasiaProtein kinase activityCell cycle checkpointsAmino acid residuesSelectable marker cassetteDetectable ATM proteinMutant proteinsATM proteinCycle checkpointsHomologous recombinationKinase activityAcid residuesMarker cassetteCommon deletion mutationsDeletion mutationsDeletion resultsCre-loxPATM geneThymic lymphomasExtensive apoptosisVariant phenotypesDifferent phenotypesFas ligand