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