2022
CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging.
Cui H, Xie N, Banerjee S, Dey T, Liu RM, Antony VB, Sanders YY, Adams TS, Gomez JL, Thannickal VJ, Kaminski N, Liu G. CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging. American Journal Of Respiratory And Critical Care Medicine 2022, 206: 459-475. PMID: 35687485, DOI: 10.1164/rccm.202109-2151oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisLung fibrosisCD38 expressionAlveolar epithelial cell injuryEpithelial cell injuryEffective therapeutic strategyHuman lung parenchymaIPF lungsLung functionPulmonary fibrosisDisease progressionFibrotic lungsReal-time PCRYoung miceLung parenchymaOld miceCell injuryTherapeutic strategiesFibrosisPharmacological inactivationCD38Single-cell RNA sequencingFlow cytometryWestern blottingOld animals
2020
Mitochondrial antiviral signaling protein is crucial for the development of pulmonary fibrosis
Kim SH, Lee JY, Yoon CM, Shin HJ, Lee SW, Rosas I, Herzog E, Dela Cruz C, Kaminski N, Kang MJ. Mitochondrial antiviral signaling protein is crucial for the development of pulmonary fibrosis. European Respiratory Journal 2020, 57: 2000652. PMID: 33093124, PMCID: PMC8559259, DOI: 10.1183/13993003.00652-2020.Peer-Reviewed Original ResearchConceptsDamage-associated molecular patternsIdiopathic pulmonary fibrosisPulmonary fibrosisMAVS aggregationMultiple damage-associated molecular patternsExperimental pulmonary fibrosisMitochondrial antiviral signaling proteinInnate immune responseIPF patientsMAVS signalingIPF treatmentBleomycin injuryLung fibrosisTherapeutic effectImmune responseTherapeutic strategiesMAVS expressionFibrosisDanger signalsCritical mediatorMolecular patternsABT-263LungInjuryBH3 mimeticsAn allosteric site on MKP5 reveals a strategy for small-molecule inhibition
Gannam Z, Min K, Shillingford SR, Zhang L, Herrington J, Abriola L, Gareiss PC, Pantouris G, Tzouvelekis A, Kaminski N, Zhang X, Yu J, Jamali H, Ellman JA, Lolis E, Anderson KS, Bennett AM. An allosteric site on MKP5 reveals a strategy for small-molecule inhibition. Science Signaling 2020, 13 PMID: 32843541, PMCID: PMC7569488, DOI: 10.1126/scisignal.aba3043.Peer-Reviewed Original ResearchMeSH KeywordsAllosteric SiteAmino Acid SequenceAnimalsCell DifferentiationCell LineDual-Specificity PhosphatasesEnzyme InhibitorsFemaleHigh-Throughput Screening AssaysHumansKineticsMiceMice, KnockoutMitogen-Activated Protein Kinase PhosphatasesMyoblastsProtein BindingSequence Homology, Amino AcidSignal TransductionSmall Molecule LibrariesConceptsDystrophic muscle diseaseMitogen-activated protein kinaseMuscle diseaseTGF-β1Promising therapeutic targetP38 mitogen-activated protein kinaseTherapeutic strategiesTherapeutic targetSmall molecule inhibitionSmad2 phosphorylationDiseasePotential targetSmall-molecule screenInhibitorsTreatmentInhibitionIntroduction
Gomez J, Kaminski N, Himes B. Introduction. Respiratory Medicine 2020, 3-8. DOI: 10.1007/978-3-030-31507-8_1.Peer-Reviewed Original Research
2016
SH2 Domain–Containing Phosphatase-2 Is a Novel Antifibrotic Regulator in Pulmonary Fibrosis
Tzouvelekis A, Yu G, Lino Cardenas CL, Herazo-Maya JD, Wang R, Woolard T, Zhang Y, Sakamoto K, Lee H, Yi JS, DeIuliis G, Xylourgidis N, Ahangari F, Lee PJ, Aidinis V, Herzog EL, Homer R, Bennett AM, Kaminski N. SH2 Domain–Containing Phosphatase-2 Is a Novel Antifibrotic Regulator in Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2016, 195: 500-514. PMID: 27736153, PMCID: PMC5378419, DOI: 10.1164/rccm.201602-0329oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisProfibrotic stimuliLung fibroblastsChronic fatal lung diseaseMyofibroblast differentiationPrimary human lung fibroblastsFatal lung diseaseNovel therapeutic strategiesVivo therapeutic effectPotential therapeutic usefulnessHuman lung fibroblastsMouse lung fibroblastsDismal prognosisFibroblastic fociLung fibrosisLung diseaseBleomycin modelTherapeutic effectTherapeutic usefulnessTherapeutic strategiesTherapeutic targetTransgenic miceFibrosisSHP2 overexpressionNovel 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
2015
Regulation of alveolar septation by microRNA-489
Olave N, Lal CV, Halloran B, Pandit K, Cuna AC, Faye-Petersen OM, Kelly DR, Nicola T, Benos PV, Kaminski N, Ambalavanan N. Regulation of alveolar septation by microRNA-489. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2015, 310: l476-l487. PMID: 26719145, PMCID: PMC4773841, DOI: 10.1152/ajplung.00145.2015.Peer-Reviewed Original ResearchConceptsBronchopulmonary dysplasiaMiR-489Alveolar septationLung developmentInsulin-like growth factor-1Abnormal lung developmentGrowth factor-1MiR-489 overexpressionNormal pretermTerm infantsC57BL/6 miceMouse lung developmentTherapeutic strategiesMiRNA-489HyperoxiaEpithelial originFurther inhibitionIGF1Factor 1MiRNA antagonistsNormoxiaTenascin CMiRNA profilesCytomegalovirus promoterInfants
2004
Blood transcriptional signatures of multiple sclerosis: Unique gene expression of disease activity
Achiron A, Gurevich M, Friedman N, Kaminski N, Mandel M. Blood transcriptional signatures of multiple sclerosis: Unique gene expression of disease activity. Annals Of Neurology 2004, 55: 410-417. PMID: 14991819, DOI: 10.1002/ana.20008.Peer-Reviewed Original ResearchConceptsPeripheral blood mononuclear cellsMultiple sclerosisMS patientsTranscriptional signatureCentral nervous system diseaseBlood transcriptional signaturesBlood mononuclear cellsNervous system diseasesT cell activationAcute relapseDisease activityImmunomodulatory treatmentMS pathogenesisActive demyelinationMononuclear cellsUnpredictable courseImmune surveillanceCellular recruitmentSystem diseasesTherapeutic strategiesDisease processDisease pathogenesisUnique gene expressionSclerosisPatients