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
2006
Essential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung
Bhandari V, Choo-Wing R, Chapoval SP, Lee CG, Tang C, Kim YK, Ma B, Baluk P, Lin MI, McDonald DM, Homer RJ, Sessa WC, Elias JA. Essential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung. Proceedings Of The National Academy Of Sciences Of The United States Of America 2006, 103: 11021-11026. PMID: 16832062, PMCID: PMC1544167, DOI: 10.1073/pnas.0601057103.Peer-Reviewed Original ResearchConceptsInducible NOSNitric oxideEndothelial NOS inhibitorDendritic cell activationNO-dependent mechanismAirway hyperresponsivenessMucus metaplasiaLymphocyte accumulationPulmonary alterationsCell hyperplasiaNOS inhibitorNormal micePhysiologic responsesCell activationInflammationENOSVEGFMiceIndependent mechanismsTissue responseLatter responseLungAngiogenesisRemodelingNull mutation