2014
The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis
Huang LS, Mathew B, Li H, Zhao Y, Ma SF, Noth I, Reddy SP, Harijith A, Usatyuk PV, Berdyshev EV, Kaminski N, Zhou T, Zhang W, Zhang Y, Rehman J, Kotha SR, Gurney TO, Parinandi NL, Lussier YA, Garcia JG, Natarajan V. The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 1402-1415. PMID: 24779708, PMCID: PMC4098083, DOI: 10.1164/rccm.201310-1917oc.Peer-Reviewed Original ResearchMeSH Keywords1-Acylglycerol-3-Phosphate O-AcyltransferaseAcyltransferasesAnimalsBiomarkersCardiolipinsCohort StudiesDisease Models, AnimalHumansIdiopathic Pulmonary FibrosisIn Situ HybridizationLeukocytes, MononuclearMiceMitochondriaPredictive Value of TestsPulmonary FibrosisRNA, MessengerSensitivity and SpecificitySeverity of Illness IndexConceptsPeripheral blood mononuclear cellsIdiopathic pulmonary fibrosisPulmonary fibrosisMurine modelAlveolar epithelial cellsOverall survivalReactive oxygen species generationLysocardiolipin acyltransferaseOxygen species generationCarbon monoxide diffusion capacityRadiation-induced pulmonary fibrosisPulmonary function outcomesEpithelial cellsBlood mononuclear cellsPreclinical murine modelsNovel therapeutic approachesSpecies generationBleomycin challengeLung inflammationLung protectionPulmonary functionFunction outcomesLung fibrosisMononuclear cellsFibrotic lungs
2011
Mouse Conjunctival Forniceal Gene Expression during Postnatal Development and Its Regulation by Krüppel-like Factor 4
Gupta D, Harvey SA, Kaminski N, Swamynathan SK. Mouse Conjunctival Forniceal Gene Expression during Postnatal Development and Its Regulation by Krüppel-like Factor 4. Investigative Ophthalmology & Visual Science 2011, 52: 4951-4962. PMID: 21398290, PMCID: PMC3176043, DOI: 10.1167/iovs.10-7068.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsConjunctivaEpithelial CellsFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalGenotypeGoblet CellsIn Situ HybridizationKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMiceOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionTranscription FactorsConceptsKLF4 target genesGene expressionTarget genesEts transcription factor family memberCell developmentTranscription factor family membersGene regulatory networksGoblet cell developmentLaser microdissectionComponents of pathwaysTranscription factor SPDEFFactor family membersMesenchymal-epithelial transitionKrüppel-like factor 4Regulatory networksRegulatory targetsRole of KLF4Spatiotemporal expressionQuantitative RT-PCRGlycoprotein biosynthesisMucosal epitheliumGoblet cellsGenesKLF4Transcripts
2010
Inhibition and Role of let-7d in Idiopathic Pulmonary Fibrosis
Pandit KV, Corcoran D, Yousef H, Yarlagadda M, Tzouvelekis A, Gibson KF, Konishi K, Yousem SA, Singh M, Handley D, Richards T, Selman M, Watkins SC, Pardo A, Ben-Yehudah A, Bouros D, Eickelberg O, Ray P, Benos PV, Kaminski N. Inhibition and Role of let-7d in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2010, 182: 220-229. PMID: 20395557, PMCID: PMC2913236, DOI: 10.1164/rccm.200911-1698oc.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCadherinsCells, CulturedDown-RegulationEpithelial CellsHMGA2 ProteinHumansIdiopathic Pulmonary FibrosisIn Situ HybridizationLungMiceMice, Inbred C57BLMicroRNAsPolymerase Chain ReactionPulmonary AlveoliS100 Calcium-Binding Protein A4S100 ProteinsSmad3 ProteinTransforming Growth Factor betaVimentinConceptsIdiopathic pulmonary fibrosisReal-time polymerase chain reactionQuantitative real-time polymerase chain reactionAlveolar epithelial cellsIPF lungsPulmonary fibrosisPolymerase chain reactionLet-7dEpithelial cellsLethal fibrotic lung diseaseAlpha-smooth muscle actinAlveolar septal thickeningMesenchymal markers N-cadherinFibrotic lung diseaseChain reactionLet-7d expressionSeptal thickeningPulmonary functionLung diseaseLung fibrosisEpithelial cell lineIntratracheal administrationIPF tissueProfibrotic effectsClinical trials
2009
FACS-Assisted Microarray Profiling Implicates Novel Genes and Pathways in Zebrafish Gastrointestinal Tract Development
Stuckenholz C, Lu L, Thakur P, Kaminski N, Bahary N. FACS-Assisted Microarray Profiling Implicates Novel Genes and Pathways in Zebrafish Gastrointestinal Tract Development. Gastroenterology 2009, 137: 1321-1332. PMID: 19563808, PMCID: PMC2785077, DOI: 10.1053/j.gastro.2009.06.050.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, Genetically ModifiedCell SeparationChromosomes, Human, Pair 8Digestive System NeoplasmsFlow CytometryGastrointestinal TractGene Expression ProfilingGene Expression Regulation, DevelopmentalGene Expression Regulation, NeoplasticGene Regulatory NetworksGreen Fluorescent ProteinsHumansIn Situ HybridizationLarvaMicroRNAsOligonucleotide Array Sequence AnalysisOrganogenesisReproducibility of ResultsTime FactorsZebrafishZebrafish ProteinsConceptsFluorescence-activated cell sortingNovel genesGreen fluorescent proteinGene networksPutative transcription factorTransgenic zebrafish lineZebrafish Danio rerioPhosphatidylinositol-3-kinase (PI3K) pathwayExcellent model systemDevelopmental time pointsChromosome arm 8qGastrointestinal developmentZebrafish lineHuman orthologDanio rerioTranscription factorsKinase pathwayMicroarray profilingFluorescent proteinGFP expressionGenesNovel pathwayGFP cellsCell sortingOrganogenesis