2016
Inhibition of Regulatory-Associated Protein of Mechanistic Target of Rapamycin Prevents Hyperoxia-Induced Lung Injury by Enhancing Autophagy and Reducing Apoptosis in Neonatal Mice
Sureshbabu A, Syed M, Das P, Janér C, Pryhuber G, Rahman A, Andersson S, Homer RJ, Bhandari V. Inhibition of Regulatory-Associated Protein of Mechanistic Target of Rapamycin Prevents Hyperoxia-Induced Lung Injury by Enhancing Autophagy and Reducing Apoptosis in Neonatal Mice. American Journal Of Respiratory Cell And Molecular Biology 2016, 55: 722-735. PMID: 27374190, PMCID: PMC5105179, DOI: 10.1165/rcmb.2015-0349oc.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAdaptor Proteins, Signal TransducingAlveolar Epithelial CellsAnimalsAnimals, NewbornApoptosisAutophagyBronchopulmonary DysplasiaCell LineFemaleHumansHyperoxiaHypertension, PulmonaryHypertrophy, Right VentricularInfant, NewbornLungMiceMicrotubule-Associated ProteinsNaphthyridinesPhenotypeRegulatory-Associated Protein of mTORTime FactorsTumor Suppressor Protein p53ConceptsAcute lung injuryBronchopulmonary dysplasiaLung injuryWild-type miceMechanistic targetRegulatory-Associated ProteinLysosomal-associated membrane protein 1Apoptotic cell deathFetal type II alveolar epithelial cellsMouse lungRole of autophagyHyperoxia-Induced Lung InjuryLight chain 3Activation of autophagyType II alveolar epithelial cellsRespiratory distress syndromeMembrane protein 1Developmental lung diseaseUseful therapeutic targetNeonatal mouse lungAlveolar epithelial cellsPharmacological inhibitorsTreatment of hyperoxiaCell deathAutophagic fluxRole of Nitric Oxide Isoforms in Vascular and Alveolar Development and Lung Injury in Vascular Endothelial Growth Factor Overexpressing Neonatal Mice Lungs
Syed MA, Choo-Wing R, Homer RJ, Bhandari V. Role of Nitric Oxide Isoforms in Vascular and Alveolar Development and Lung Injury in Vascular Endothelial Growth Factor Overexpressing Neonatal Mice Lungs. PLOS ONE 2016, 11: e0147588. PMID: 26799210, PMCID: PMC4723240, DOI: 10.1371/journal.pone.0147588.Peer-Reviewed Original ResearchConceptsVascular endothelial growth factorEndothelial growth factorVascular markersRoom airVascular permeabilityMouse lungLung developmentVEGF overexpressionDifferent nitric oxide synthase isoformsNitric oxide synthase isoformsGrowth factorInhibition of NOS1Inhibition of NOS2Nitric oxide isoformsOxidative stress markersNeonatal mouse lungNOS1 inhibitionNOS1 inhibitorInjury markersLung injuryLung vascularNewborn lungNOS pathwayAlveolar developmentPostnatal day
2015
Conditional overexpression of TGFβ1 promotes pulmonary inflammation, apoptosis and mortality via TGFβR2 in the developing mouse lung
Sureshbabu A, Syed MA, Boddupalli CS, Dhodapkar MV, Homer RJ, Minoo P, Bhandari V. Conditional overexpression of TGFβ1 promotes pulmonary inflammation, apoptosis and mortality via TGFβR2 in the developing mouse lung. Respiratory Research 2015, 16: 4. PMID: 25591994, PMCID: PMC4307226, DOI: 10.1186/s12931-014-0162-6.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAlveolar Epithelial CellsAnimalsAnimals, NewbornApoptosisDisease Models, AnimalGenotypeHumansHyperoxiaLungMice, Inbred C57BLMice, KnockoutMice, TransgenicPhenotypePneumoniaProtein Serine-Threonine KinasesReceptor, Transforming Growth Factor-beta Type IIReceptors, Transforming Growth Factor betaSignal TransductionTime FactorsTransforming Growth Factor beta1Up-RegulationConceptsImpaired alveolarizationBronchopulmonary dysplasiaAlveolar epithelial cellsPulmonary inflammationPulmonary phenotypeMouse lungAcute lung injuryType II alveolar epithelial cellsApoptotic cell deathCell deathNewborn mouse lungPotential therapeutic strategyGrowth factor betaNull mutant miceLung injuryImproved survivalNeonatal mortalityMonocyte infiltrationAbnormal alveolarizationAngiogenic mediatorsInflammatory signalsTGFβ1 expressionTherapeutic strategiesInflammatory macrophagesLung morphometry
2013
Hyperoxia and Interferon-γ–Induced Injury in Developing Lungs Occur via Cyclooxygenase-2 and the Endoplasmic Reticulum Stress–Dependent Pathway
Choo-Wing R, Syed MA, Harijith A, Bowen B, Pryhuber G, Janér C, Andersson S, Homer RJ, Bhandari V. Hyperoxia and Interferon-γ–Induced Injury in Developing Lungs Occur via Cyclooxygenase-2 and the Endoplasmic Reticulum Stress–Dependent Pathway. American Journal Of Respiratory Cell And Molecular Biology 2013, 48: 749-757. PMID: 23470621, PMCID: PMC3727872, DOI: 10.1165/rcmb.2012-0381oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornBronchopulmonary DysplasiaCelecoxibCell DeathCyclooxygenase 2Cyclooxygenase 2 InhibitorsEndoplasmic Reticulum StressHumansHyperoxiaImmunohistochemistryInfant, NewbornInterferon-gammaLungMiceMice, Inbred C57BLMice, TransgenicPyrazolesRNA, Small InterferingSulfonamidesTranscription Factor CHOPConceptsBronchopulmonary dysplasiaCyclooxygenase-2Endoplasmic reticulum stress-dependent pathwaysER stress pathway activationPathway mediatorsHuman bronchopulmonary dysplasiaFinal common pathwayAlveolar epithelial cellsImpaired alveolarizationStress pathway activationCOX2 inhibitionMurine modelMurine lungClinical relevanceIFNVivo modelHyperoxiaLungHuman lungPathway activationCHOP siRNAStress-dependent pathwaysInjuryEpithelial cellsCommon pathway
2008
Developmental Regulation of NO-Mediated VEGF-Induced Effects in the Lung
Bhandari V, Choo-Wing R, Lee CG, Yusuf K, Nedrelow JH, Ambalavanan N, Malkus H, Homer RJ, Elias JA. Developmental Regulation of NO-Mediated VEGF-Induced Effects in the Lung. American Journal Of Respiratory Cell And Molecular Biology 2008, 39: 420-430. PMID: 18441284, PMCID: PMC2551703, DOI: 10.1165/rcmb.2007-0024oc.Peer-Reviewed Original ResearchMeSH KeywordsAmniotic FluidAnimalsAnimals, NewbornBronchopulmonary DysplasiaCapillary PermeabilityFemaleHemorrhageHumansHyperoxiaInfant, NewbornLungLung DiseasesMiceMice, TransgenicNitric OxidePregnancyPulmonary SurfactantsRespiratory Distress Syndrome, NewbornTracheaVascular Endothelial Growth Factor AConceptsVascular endothelial growth factorVEGF levelsLung developmentNitric oxide mediationNO-dependent mechanismAdult murine lungPotential clinical benefitTransgenic murine modelSignificant differencesEndothelial growth factorBronchopulmonary dysplasiaLung injuryPulmonary hemorrhageCytokine responsesClinical benefitNeonatal lungHuman neonatesMurine modelMurine lungMature lungLungPathologic conditionsAdult lungSurfactant phospholipidsExtravascular effects
2007
Developmental differences in the responses of IL-6 and IL-13 transgenic mice exposed to hyperoxia
Choo-Wing R, Nedrelow JH, Homer RJ, Elias JA, Bhandari V. Developmental differences in the responses of IL-6 and IL-13 transgenic mice exposed to hyperoxia. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2007, 293: l142-l150. PMID: 17400600, DOI: 10.1152/ajplung.00434.2006.Peer-Reviewed Original ResearchConceptsIL-13 transgenic miceIL-6Transgenic miceTracheal aspirate levelsWild-type littermate controlsIL-6 levelsRespiratory distress syndromeAngiogenic factor expressionLung injuryDistress syndromePremature neonatesTracheal aspiratesAdverse outcomesIL-13Human neonatesProtective effectSurvival advantageLittermate controlsAdult miceClinical relevanceTUNEL stainingCytoprotective effectsNewborn animalsMature miceFactor expression
1997
Regulated overexpression of interleukin 11 in the lung. Use to dissociate development-dependent and -independent phenotypes.
Ray P, Tang W, Wang P, Homer R, Kuhn C, Flavell RA, Elias JA. Regulated overexpression of interleukin 11 in the lung. Use to dissociate development-dependent and -independent phenotypes. Journal Of Clinical Investigation 1997, 100: 2501-2511. PMID: 9366564, PMCID: PMC508450, DOI: 10.1172/jci119792.Peer-Reviewed Original Research