2024
Context‐specific anti‐inflammatory roles of type III interferon signaling in the lung in nonviral injuries
Feng J, Kim J, Wang V, Chang D, Liu H, Bain W, Robinson K, Jie Z, Kotenko S, Dela Cruz C, Sharma L. Context‐specific anti‐inflammatory roles of type III interferon signaling in the lung in nonviral injuries. Physiological Reports 2024, 12: e70104. PMID: 39455422, PMCID: PMC11511623, DOI: 10.14814/phy2.70104.Peer-Reviewed Original ResearchConceptsIII interferon signalingType III interferon signalingLung injuryInterferon signalingBleomycin-induced weight lossInflammatory responseModel of lung injuryBacterial pathogen Pseudomonas aeruginosaAcute lung injuryPathogen Pseudomonas aeruginosaBacterial endotoxin LPSChemotherapeutic agent bleomycinType III interferonsAnti-inflammatory roleIncreased inflammatory signalingLate time pointsBleomycin modelKnockout miceEndotoxin LPSIII interferonsAntiviral cytokinesDay 3Inflammatory signalingEarly injuryImpaired recovery
2022
Epidermal Growth Factor Receptor Inhibition Is Protective in Hyperoxia‐Induced Lung Injury
Harris ZM, Sun Y, Joerns J, Clark B, Hu B, Korde A, Sharma L, Shin HJ, Manning EP, Placek L, Unutmaz D, Stanley G, Chun H, Sauler M, Rajagopalan G, Zhang X, Kang MJ, Koff JL. Epidermal Growth Factor Receptor Inhibition Is Protective in Hyperoxia‐Induced Lung Injury. Oxidative Medicine And Cellular Longevity 2022, 2022: 9518592. PMID: 36193076, PMCID: PMC9526641, DOI: 10.1155/2022/9518592.Peer-Reviewed Original ResearchConceptsAcute lung injuryEpidermal growth factor receptorAlveolar epithelial cellsLung injurySevere hyperoxiaEGFR inhibitionEpithelial cellsHyperoxia-Induced Lung InjuryRole of EGFRMurine alveolar epithelial cellsGrowth factor receptor inhibitionWorse clinical outcomesEpidermal growth factor receptor inhibitionHuman alveolar epithelial cellsWild-type littermatesPoly (ADP-ribose) polymeraseTerminal dUTP nickGrowth factor receptorClinical outcomesImproved survivalReceptor inhibitionLung repairProtective roleComplex roleEGFR deletion
2016
IL-13Rα2 uses TMEM219 in chitinase 3-like-1-induced signalling and effector responses
Lee CM, He CH, Nour AM, Zhou Y, Ma B, Park JW, Kim KH, Cruz CD, Sharma L, Nasr ML, Modis Y, Lee CG, Elias JA. IL-13Rα2 uses TMEM219 in chitinase 3-like-1-induced signalling and effector responses. Nature Communications 2016, 7: 12752. PMID: 27629921, PMCID: PMC5027616, DOI: 10.1038/ncomms12752.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell Line, TumorChitinase-3-Like Protein 1Heparin-binding EGF-like Growth FactorHumansInterleukin-13 Receptor alpha2 SubunitLung InjuryLung NeoplasmsMAP Kinase Signaling SystemMelanoma, ExperimentalMembrane ProteinsMice, Inbred C57BLNeoplasm MetastasisProto-Oncogene Proteins c-aktTransforming Growth Factor beta1Two-Hybrid System TechniquesWnt Signaling PathwayConceptsNull mutationPKB/Akt activationBimolecular fluorescence complementationDirect physical interactionMAPK/ERKHB-EGF productionFluorescence complementationTwo-hybridMembrane proteinsAkt activationDecoy functionPhysical interactionIL-13Rα2Effect of CHI3L1Chitinase 3Critical roleSignalingMutationsRecent studiesCHI3L1ComplementationTGF-β1YeastMelanoma metastasesERK