2024
Succinate dehydrogenase–complex II regulates skeletal muscle cellular respiration and contractility but not muscle mass in genetically induced pulmonary emphysema
Balnis J, Tufts A, Jackson E, Drake L, Singer D, Lacomis D, Lee C, Elias J, Doles J, Maher L, Jen A, Coon J, Jourd’heuil D, Singer H, Vincent C, Jaitovich A. Succinate dehydrogenase–complex II regulates skeletal muscle cellular respiration and contractility but not muscle mass in genetically induced pulmonary emphysema. Science Advances 2024, 10: eado8549. PMID: 39167644, PMCID: PMC11338223, DOI: 10.1126/sciadv.ado8549.Peer-Reviewed Original ResearchConceptsPulmonary emphysemaMuscle massSuccinate dehydrogenaseReduced skeletal muscle massAssociated with high mortalityCellular respirationSkeletal muscle massReduced cellular respirationKnockout miceMuscle dysfunctionActivity of succinate dehydrogenaseComplex I respirationMitochondrial oxygen consumptionMyopathic changesTransgenic miceSubunit cMuscle atrophyProteomic effectsMyofiber contractilityRespirometry analysisSuccinate accumulationMuscle mitochondriaEmphysemaHigher mortalityAnimal data
2009
Role of breast regression protein 39 (BRP-39)/chitinase 3-like-1 in Th2 and IL-13–induced tissue responses and apoptosis
Lee CG, Hartl D, Lee GR, Koller B, Matsuura H, Da Silva CA, Sohn MH, Cohn L, Homer RJ, Kozhich AA, Humbles A, Kearley J, Coyle A, Chupp G, Reed J, Flavell RA, Elias JA. Role of breast regression protein 39 (BRP-39)/chitinase 3-like-1 in Th2 and IL-13–induced tissue responses and apoptosis. Journal Of Experimental Medicine 2009, 206: 1149-1166. PMID: 19414556, PMCID: PMC2715037, DOI: 10.1084/jem.20081271.Peer-Reviewed Original ResearchConceptsBRP-39/YKLBreast regression protein 39YKL-40BRP-39Th2 responsesIL-13-induced tissue responsesDendritic cell accumulationAlternative macrophage activationApoptosis/cell deathProtein 39Protein kinase B/AktTh2 inflammationDisease activityAntigen sensitizationEffector phaseTissue inflammationExaggerated quantitiesPulmonary epitheliumTherapeutic targetMacrophage activationTransgenic miceCell accumulationFas expressionNovel regulatory roleMice
2008
Cigarette smoke selectively enhances viral PAMP– and virus-induced pulmonary innate immune and remodeling responses in mice
Kang MJ, Lee CG, Lee JY, Dela Cruz CS, Chen ZJ, Enelow R, Elias JA. Cigarette smoke selectively enhances viral PAMP– and virus-induced pulmonary innate immune and remodeling responses in mice. Journal Of Clinical Investigation 2008, 118: 2771-2784. PMID: 18654661, PMCID: PMC2483678, DOI: 10.1172/jci32709.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseMitochondrial antiviral signaling proteinCigarette smokeDisease exacerbationIFN-gammaInnate immunityViral PAMPsEffects of CSIL-12/ILSevere disease exacerbationsObstructive pulmonary diseaseEffects of influenzaType I IFNAirway fibrosisAirway inflammationLung functionPulmonary diseasePulmonary inflammationIL-18IL-18RalphaI IFNMurine lungViral infectionInflammationRNA-dependent protein kinase
2003
Adenosine mediates IL-13–induced inflammation and remodeling in the lung and interacts in an IL-13–adenosine amplification pathway
Blackburn MR, Lee CG, Young HW, Zhu Z, Chunn JL, Kang MJ, Banerjee SK, Elias JA. Adenosine mediates IL-13–induced inflammation and remodeling in the lung and interacts in an IL-13–adenosine amplification pathway. Journal Of Clinical Investigation 2003, 112: 332-344. PMID: 12897202, PMCID: PMC166289, DOI: 10.1172/jci16815.Peer-Reviewed Original ResearchConceptsIL-13-induced inflammationIL-13Adenosine receptorsAdenosine accumulationIL-13-induced tissue responsesADA enzyme therapyIL-13 overexpressionTh2-mediated disordersIL-13-induced increaseAmplification pathwayAdenosine deaminase activityLevels of adenosineA2A adenosine receptorsAlveolar destructionRespiratory failureMurine lungEnzyme therapyADA activityRemodeling responseImportant mediatorInflammationLungReceptorsProgressive increaseTissue response