2015
Mitochondrial Regulation of Inflammasome Activation in Chronic Obstructive Pulmonary Disease
Yoon CM, Nam M, Oh YM, Dela Cruz CS, Kang MJ. Mitochondrial Regulation of Inflammasome Activation in Chronic Obstructive Pulmonary Disease. Journal Of Innate Immunity 2015, 8: 121-128. PMID: 26536345, PMCID: PMC4801739, DOI: 10.1159/000441299.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsHumansImmunity, InnateInflammasomesInflammationMitochondriaPulmonary Disease, Chronic ObstructiveSignal TransductionSmokingConceptsChronic obstructive pulmonary diseaseObstructive pulmonary diseaseCigarette smokeInflammasome activationPulmonary diseaseInflammatory responsePathogenesis of COPDMajor unmet medical needLung inflammatory responseUnmet medical needInnate immune signalingChronic airwayImmune driversPulmonary inflammationCOPD pathogenesisNoxious particlesMedical needImmune signalingInflammationPathogenesisDiseaseActivationCentral playerResponseAirway
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
2010
Role of Breast Regression Protein–39 in the Pathogenesis of Cigarette Smoke–Induced Inflammation and Emphysema
Matsuura H, Hartl D, Kang MJ, Dela Cruz CS, Koller B, Chupp GL, Homer RJ, Zhou Y, Cho WK, Elias JA, Lee CG. Role of Breast Regression Protein–39 in the Pathogenesis of Cigarette Smoke–Induced Inflammation and Emphysema. American Journal Of Respiratory Cell And Molecular Biology 2010, 44: 777-786. PMID: 20656949, PMCID: PMC3135840, DOI: 10.1165/rcmb.2010-0081oc.Peer-Reviewed Original ResearchMeSH KeywordsAdipokinesAgedAnimalsChitinase-3-Like Protein 1EmphysemaFemaleGlycoproteinsHumansInflammationInterleukin-18LectinsLungMaleMiceMice, Inbred C57BLMice, TransgenicMiddle AgedPulmonary Disease, Chronic ObstructiveSignal TransductionSmokeSmokingConceptsChronic obstructive pulmonary diseaseBRP-39/YKLBreast regression protein 39YKL-40BRP-39Alveolar destructionCigarette smokeChitinase-like protein YKL-40Emphysematous alveolar destructionLungs of CSObstructive pulmonary diseaseProtein YKL-40Excessive inflammatory responseAirway epithelial cellsAlveolar type II cellsNull mutant miceProtein 39Epithelial cell apoptosisType II cellsCurrent smokersPulmonary diseaseBronchoalveolar lavageTissue inflammationEmphysematous destructionSerum concentrations