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
2018
Hypercapnia 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
2016
Novel Mechanisms of Disease: Network Biology and MicroRNA Signaling in Pulmonary Hypertension
Fares W, Pandit K, Kaminski N. Novel Mechanisms of Disease: Network Biology and MicroRNA Signaling in Pulmonary Hypertension. 2016, 123-133. DOI: 10.1007/978-3-319-23594-3_7.Peer-Reviewed Original ResearchPulmonary arterial hypertensionSmall non-coding RNAsNon-coding RNAsRole of microRNAsNumerous genesNetwork biologyGene expressionPhysiological processesVascular remodeling diseaseArtery smooth muscle cellsPulmonary artery smooth muscle cellsProgression of PAHMicroRNA signallingNovel mechanismMicroRNAsSmooth muscle cellsRight heart failureMuscle cellsArterial hypertensionPulmonary hypertensionHeart failureEndothelial cellsArterial remodelingHistological changesTherapeutic strategies
2007
Accelerated Variant of Idiopathic Pulmonary Fibrosis: Clinical Behavior and Gene Expression Pattern
Selman M, Carrillo G, Estrada A, Mejia M, Becerril C, Cisneros J, Gaxiola M, Pérez-Padilla R, Navarro C, Richards T, Dauber J, King TE, Pardo A, Kaminski N. Accelerated Variant of Idiopathic Pulmonary Fibrosis: Clinical Behavior and Gene Expression Pattern. PLOS ONE 2007, 2: e482. PMID: 17534432, PMCID: PMC1868965, DOI: 10.1371/journal.pone.0000482.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisMonths of symptomsSubset of patientsRapid progressorsPulmonary fibrosisProgression of IPFBronchoalveolar lavage (BAL) cellular profileActive matrix metalloproteinase-9Kaplan-Meyer methodRapid progressor groupTime of diagnosisBeginning of symptomsEnd-stage diseaseAccelerated clinical courseMatrix metalloproteinase-9Proportional hazards modelMigration/proliferationAdenosine 2B receptorSmooth muscle cellsAlveolar epithelial cellsIPF patientsProgressor groupSlow progressorsClinical courseInsidious onset
2001
Interleukin-13 Induces Dramatically Different Transcriptional Programs in Three Human Airway Cell Types
Lee J, Kaminski N, Dolganov G, Grunig G, Koth L, Solomon C, Erle D, Sheppard D. Interleukin-13 Induces Dramatically Different Transcriptional Programs in Three Human Airway Cell Types. American Journal Of Respiratory Cell And Molecular Biology 2001, 25: 474-485. PMID: 11694453, DOI: 10.1165/ajrcmb.25.4.4522.Peer-Reviewed Original ResearchMeSH KeywordsCells, CulturedEndopeptidasesExtracellular Matrix ProteinsFibroblastsGene Expression RegulationHumansInterleukin-13Ion ChannelsMuscle, SmoothOligonucleotide Array Sequence AnalysisProtease InhibitorsRespiratory MucosaRespiratory SystemSignal TransductionSTAT6 Transcription FactorTrans-ActivatorsTranscription, GeneticConceptsAirway cell typesIL-13Airway epithelial cellsAirway cellsAirway smooth muscle cellsPhenotypic featuresInterleukin-13 inducesResident airway cellsEpithelial cellsImmediate hypersensitivity responsesAirway smooth muscleDevelopment of asthmaCell typesSmooth muscle cellsHypersensitivity responseT lymphocytesSmooth muscleAsthmaB lymphocytesLung fibroblastsMuscle cellsVivo responseCentral mediatorGene expressionPrimary cultures