Featured Publications
A lung targeted miR-29 mimic as a therapy for pulmonary fibrosis
Chioccioli M, Roy S, Newell R, Pestano L, Dickinson B, Rigby K, Herazo-Maya J, Jenkins G, Ian S, Saini G, Johnson SR, Braybrooke R, Yu G, Sauler M, Ahangari F, Ding S, DeIuliis J, Aurelien N, Montgomery RL, Kaminski N. A lung targeted miR-29 mimic as a therapy for pulmonary fibrosis. EBioMedicine 2022, 85: 104304. PMID: 36265417, PMCID: PMC9587275, DOI: 10.1016/j.ebiom.2022.104304.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisNon-human primatesPulmonary fibrosisAnimal modelsPro-fibrotic genesAnti-fibrotic efficacyMiR-29 mimicsHuman peripheral bloodMiR-29b levelsHuman lung fibroblastsIPF patientsIPF diagnosisPeripheral bloodReduced fibrosisAdverse findingsPotential therapyLung slicesTGF-β1Relevant dosesLung fibroblastsNIH-NHLBIFibrosisTherapyCollagen productionProfibrotic gene program
2023
Vascular-Parenchymal Cross-Talk Promotes Lung Fibrosis through BMPR2 Signaling.
Yanagihara T, Tsubouchi K, Zhou Q, Chong M, Otsubo K, Isshiki T, Schupp J, Sato S, Scallan C, Upagupta C, Revill S, Ayoub A, Chong S, Dvorkin-Gheva A, Kaminski N, Tikkanen J, Keshavjee S, Paré G, Guignabert C, Ask K, Kolb M. Vascular-Parenchymal Cross-Talk Promotes Lung Fibrosis through BMPR2 Signaling. American Journal Of Respiratory And Critical Care Medicine 2023, 207: 1498-1514. PMID: 36917778, DOI: 10.1164/rccm.202109-2174oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisVascular smooth muscle cellsAdvanced idiopathic pulmonary fibrosisPulmonary hypertensionFibrotic lungsVascular remodelingEndothelial cellsPulmonary fibrosisLung diseaseLung fibrosisDevelopment of PHConcomitant pulmonary hypertensionProgressive lung scarringPulmonary vascular remodelingFibrotic lung diseaseProgression of fibrosisActivation of VSMCsActive TGF-β1Fatal lung diseaseSmooth muscle cellsWhole-exome sequencingLung scarringEndothelial dysfunctionPoor prognosisFibrogenic effects
2020
Platform Effects on Regeneration by Pulmonary Basal Cells as Evaluated by Single-Cell RNA Sequencing
Greaney AM, Adams TS, Raredon M, Gubbins E, Schupp JC, Engler AJ, Ghaedi M, Yuan Y, Kaminski N, Niklason LE. Platform Effects on Regeneration by Pulmonary Basal Cells as Evaluated by Single-Cell RNA Sequencing. Cell Reports 2020, 30: 4250-4265.e6. PMID: 32209482, PMCID: PMC7175071, DOI: 10.1016/j.celrep.2020.03.004.Peer-Reviewed Original ResearchConceptsSingle-cell RNA sequencingBasal marker expressionBasal cellsChronic pulmonary diseaseRat tracheal epitheliumPulmonary diseaseRNA sequencingCell-based therapiesRat tracheaAir-liquid interfaceTissue graftMarker expressionTracheal epitheliumRegenerative outcomesTracheaEpithelial progenitorsDifferential outcomesEpitheliumOutcomesWhole organPopulation level
2012
Cytokine-Like Factor 1 Gene Expression Is Enriched in Idiopathic Pulmonary Fibrosis and Drives the Accumulation of CD4+ T Cells in Murine Lungs Evidence for an Antifibrotic Role in Bleomycin Injury
Kass DJ, Yu G, Loh KS, Savir A, Borczuk A, Kahloon R, Juan-Guardela B, Deiuliis G, Tedrow J, Choi J, Richards T, Kaminski N, Greenberg SM. Cytokine-Like Factor 1 Gene Expression Is Enriched in Idiopathic Pulmonary Fibrosis and Drives the Accumulation of CD4+ T Cells in Murine Lungs Evidence for an Antifibrotic Role in Bleomycin Injury. American Journal Of Pathology 2012, 180: 1963-1978. PMID: 22429962, PMCID: PMC3354590, DOI: 10.1016/j.ajpath.2012.01.010.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAnimalsBleomycinCD4-Positive T-LymphocytesCiliary Neurotrophic Factor Receptor alpha SubunitCollagenDrug InteractionsEpithelial CellsGene Expression ProfilingHumansIdiopathic Pulmonary FibrosisMacrophages, AlveolarMaleMicePulmonary AlveoliRatsRats, Sprague-DawleyReceptors, CytokineRecombinant ProteinsRNA, MessengerUp-RegulationConceptsIdiopathic pulmonary fibrosisType II alveolar epithelial cellsCytokine receptor-like factor 1Alveolar epithelial cellsPulmonary fibrosisCardiotrophin-like cytokineCiliary neurotrophic factor receptorIPF lungsT cellsEpithelial cellsPathogenesis of IPFAccumulation of CD4IL-6 family membersExperimental pulmonary fibrosisFatal lung diseaseNeurotrophic factor receptorAntifibrotic responsesIPF pathogenesisT helperPulmonary accumulationBleomycin injuryInterleukin-6 familyLung diseaseAntifibrotic roleCytokine interferon
2011
Matrix Metalloproteinase 3 Is a Mediator of Pulmonary Fibrosis
Yamashita CM, Dolgonos L, Zemans RL, Young SK, Robertson J, Briones N, Suzuki T, Campbell MN, Gauldie J, Radisky DC, Riches DW, Yu G, Kaminski N, McCulloch CA, Downey GP. Matrix Metalloproteinase 3 Is a Mediator of Pulmonary Fibrosis. American Journal Of Pathology 2011, 179: 1733-1745. PMID: 21871427, PMCID: PMC3181358, DOI: 10.1016/j.ajpath.2011.06.041.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsBeta CateninBleomycinCadherinsCyclin D1Disease Models, AnimalEpithelial CellsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, EnzymologicGenetic VectorsHumansLungMatrix Metalloproteinase 2Matrix Metalloproteinase 3Matrix Metalloproteinase 9MiceMice, Inbred C57BLProtein TransportPulmonary FibrosisRatsRats, Sprague-DawleyRNA, MessengerSignal TransductionTransforming Growth Factor betaConceptsIdiopathic pulmonary fibrosisMatrix metalloproteinase-3Pathogenesis of IPFPulmonary fibrosisEpithelial-mesenchymal transitionMetalloproteinase-3Recombinant MMP-3Accumulation of myofibroblastsΒ-cateninCultured lung epithelial cellsAberrant repair processProliferation of myofibroblastsAdenoviral vector-mediated expressionMMP-3 expressionLung epithelial cellsCyclin D1 expressionVector-mediated expressionQuantitative RT-PCRWestern blot analysisΒ-catenin signalingEpithelial injuryLung architectureVitro treatmentRat lungFibrosis
2008
Network analysis of temporal effects of intermittent and sustained hypoxia on rat lungs
Wu W, Dave NB, Yu G, Strollo PJ, Kovkarova-Naumovski E, Ryter SW, Reeves SR, Dayyat E, Wang Y, Choi AM, Gozal D, Kaminski N. Network analysis of temporal effects of intermittent and sustained hypoxia on rat lungs. Physiological Genomics 2008, 36: 24-34. PMID: 18826996, PMCID: PMC2604785, DOI: 10.1152/physiolgenomics.00258.2007.Peer-Reviewed Original ResearchConceptsSystems biology approachEstrogen receptor 1Lung responseQuantitative real-time PCRRat lungBiology approachIntermittent hypoxiaExpression patternsSustained hypoxiaReal-time PCRDistinct gene expression patternsDifferent temporal expression patternsDownstream physiological effectsGene expression patternsTemporal expression patternsSteroid hormone receptor activityGene expression profilesTemporal expression changesRegulatory networksHormone receptor activityPulmonary hypertensionKey proteinsGene expressionMolecular networksExpression changes
2007
Towards Systems Biology of Human Pulmonary Fibrosis
Studer SM, Kaminski N. Towards Systems Biology of Human Pulmonary Fibrosis. Annals Of The American Thoracic Society 2007, 4: 85-91. PMID: 17202296, PMCID: PMC2647618, DOI: 10.1513/pats.200607-139jg.Peer-Reviewed Original ResearchConceptsSystems biology approachBiology approachSystems biologyHigh-throughput genotypingHigh-throughput technologiesMicroarray resultsBiological processesQuantitative phenotypingEnvironmental stimuliFibrosis researchMultiple pathwaysLung phenotypeBiologyGlobal analysisHuman pulmonary fibrosisGenetic polymorphismsIdiopathic pulmonary fibrosisComputational toolsPulmonary fibrosisSystemwide viewHigh-resolution profilesPhenotypePathwayLethal lung diseasePolymorphism
2006
Multiple Imprinted and Stemness Genes Provide a Link between Normal and Tumor Progenitor Cells of the Developing Human Kidney
Dekel B, Metsuyanim S, Schmidt-Ott KM, Fridman E, Jacob-Hirsch J, Simon A, Pinthus J, Mor Y, Barasch J, Amariglio N, Reisner Y, Kaminski N, Rechavi G. Multiple Imprinted and Stemness Genes Provide a Link between Normal and Tumor Progenitor Cells of the Developing Human Kidney. Cancer Research 2006, 66: 6040-6049. PMID: 16778176, DOI: 10.1158/0008-5472.can-05-4528.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsGene Expression ProfilingGenomic ImprintingHomeodomain ProteinsHumansKidneyKidney NeoplasmsMiceMice, Inbred BALB CMice, NudeMice, SCIDMultigene FamilyMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsNeoplasm TransplantationNeoplastic Stem CellsOligonucleotide Array Sequence AnalysisRatsTransplantation, HeterologousWilms TumorConceptsProgenitor cell populationsRenal progenitor cell populationStemness genesCell populationsNormal kidney developmentAdult mouse kidneyHomeobox genesMetanephric blastemaExpression of Peg3Transcriptional profilingOligonucleotide microarraysKidney developmentDifferentiated cellsCell differentiationHuman fetal kidneyTumor progenitor cellsGenesReal-time PCRMouse nephrogenesisBlastemaWT samplesProgenitor cellsStromal phenotypeWT sourcesPeg3
2005
Ha-rasval12 induces HSP70b transcription via the HSE/HSF1 system, but HSP70b expression is suppressed in Ha-rasval12-transformed cells
Stanhill A, Levin V, Hendel A, Shachar I, Kazanov D, Arber N, Kaminski N, Engelberg D. Ha-rasval12 induces HSP70b transcription via the HSE/HSF1 system, but HSP70b expression is suppressed in Ha-rasval12-transformed cells. Oncogene 2005, 25: 1485-1495. PMID: 16278678, DOI: 10.1038/sj.onc.1209193.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAnimalsCell Line, TransformedDNA-Binding ProteinsGene Expression RegulationGenes, ReporterHeat Shock Transcription FactorsHeLa CellsHSP70 Heat-Shock ProteinsHumansMiceMice, NudeNIH 3T3 CellsOncogene Protein p21(ras)Oxidation-ReductionPhosphorylationRatsTranscription FactorsTranscription, GeneticConceptsCellular protective responseHeat shock factor 1Shock factor 1Fibroblast expressionProtective responseHeat shock proteinsHSP70 expressionFactor 1Promoter-driven reporter geneSoft agarTumorsHeat shock elementShock proteinsHSF1 activationCellsDirect effectExpressionHsp70 transcriptionPoint mutations
1995
Dopamine increases renal medullary blood flow without improving regional hypoxia.
Heyman SN, Kaminski N, Brezis M. Dopamine increases renal medullary blood flow without improving regional hypoxia. Nephron 1995, 3: 331-7. PMID: 8528677.Peer-Reviewed Original ResearchConceptsMedullary blood flowMedullary PO2Blood flowOuter medullary blood flowRenal medullary blood flowOuter medullary flowVolume-expanded ratsEffects of dopamineLaser Doppler probeCortical flowIntrarenal microcirculationMedullary flowRenal microcirculationMedullary hypoxiaAnesthetized ratsRegional hypoxiaRatsDopamineMicrocirculationHypoxiaPO2Indomethacin
1990
Effects of Perfusion Pressure and Renal Flow upon Albumin Excretion in Isolated Perfused Kidneys
Raz E, Kaminski N, Brezis M. Effects of Perfusion Pressure and Renal Flow upon Albumin Excretion in Isolated Perfused Kidneys. Nephron 1990, 56: 396-398. PMID: 2079998, DOI: 10.1159/000186182.Peer-Reviewed Original ResearchConceptsGlomerular filtration rateAlbumin excretionPerfusion pressureRenal flowWhole-kidney hemodynamicsUrinary albumin excretionMicrograms/minIsolated Perfused KidneyRenal hemodynamicsAngiotensin IIKidney hemodynamicsPerfused KidneyFiltration rateRenal excretionFractional clearanceRat kidneyExcretionKidneySequential changesHemodynamicsMinAlbuminHg