2011
RIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism
Ma B, Dela Cruz CS, Hartl D, Kang MJ, Takyar S, Homer RJ, Lee CG, Elias JA. RIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism. American Journal Of Respiratory And Critical Care Medicine 2011, 183: 1322-1335. PMID: 21278304, PMCID: PMC3114061, DOI: 10.1164/rccm.201008-1276oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDEAD Box Protein 58DEAD-box RNA HelicasesDisease Models, AnimalEdemaFocal Adhesion Protein-Tyrosine KinasesImmunity, InnateInflammationInterferon Type IMiceMice, TransgenicMitogen-Activated Protein KinasesNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasePoly I-CPulmonary Disease, Chronic ObstructiveToll-Like Receptor 3Vascular Endothelial Growth Factor AConceptsVascular endothelial growth factorType 2 inflammationChronic obstructive pulmonary disease exacerbationsObstructive pulmonary disease exacerbationsChronic obstructive pulmonary diseaseViral pathogen-associated molecular patternsEndothelial nitric oxide synthaseRIG-like helicasePulmonary disease exacerbationsObstructive pulmonary diseasePathogenesis of asthmaRespiratory syncytial virusNormal pulmonary physiologyNitric oxide synthaseAntiviral innate immunityPathogen-associated molecular patternsReceptor-dependent pathwayTissue responseEndothelial growth factorVEGF receptor 1Ability of VEGFDisease exacerbationPulmonary diseaseRespiratory virusesControl mice
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 mutationRole of Early Growth Response-1 (Egr-1) in Interleukin-13-induced Inflammation and Remodeling*
Cho SJ, Kang MJ, Homer RJ, Kang HR, Zhang X, Lee PJ, Elias JA, Lee CG. Role of Early Growth Response-1 (Egr-1) in Interleukin-13-induced Inflammation and Remodeling*. Journal Of Biological Chemistry 2006, 281: 8161-8168. PMID: 16439363, DOI: 10.1074/jbc.m506770200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBronchoalveolar LavageCaspasesCell DeathCollagenDNAEarly Growth Response Protein 1Enzyme InhibitorsFibrosisFlavonoidsImmunoblottingIn Situ Nick-End LabelingInflammationInterleukin-13LungMatrix Metalloproteinase 9MiceMice, Inbred C57BLMice, TransgenicMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Models, BiologicalModels, StatisticalRNARNA, MessengerSTAT6 Transcription FactorTh2 CellsTime FactorsTransforming Growth Factor betaTransforming Growth Factor beta1TransgenesConceptsIL-13Early growth response 1IL-13-induced tissue responsesEgr-1Transgenic IL-13Matrix metalloproteinase-9Wild-type miceResponse 1Th2 inflammationCXC chemokinesMetalloproteinase-9Type miceMetalloproteinase-1Transgenic miceAlveolar remodelingTissue inhibitorInflammationPotent stimulatorImportant stimulatorMiceTissue effectsKey roleTissue responsePathogenesisApoptosis regulator