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
2021
Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response
Ranjan K, Hedl M, Sinha S, Zhang X, Abraham C. Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response. Journal Of Clinical Investigation 2021, 131: e145472. PMID: 34623328, PMCID: PMC8409591, DOI: 10.1172/jci145472.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 6AnimalsEndoplasmic Reticulum StressGenetic VariationHost Microbial InteractionsHumansImmunity, InnateInflammatory Bowel DiseasesMacrophagesMiceMice, Inbred C57BLMice, KnockoutNod2 Signaling Adaptor ProteinReceptors, Pattern RecognitionRisk FactorsSignal TransductionUbiquitinationUbiquitin-Protein LigasesUnfolded Protein ResponseConceptsPattern recognition receptorsUnfolded protein responseInflammatory bowel diseaseER stress sensorsHuman macrophagesIntestinal immune homeostasisProtein responseInnate immune systemRisk variantsKey macrophage functionsBowel diseaseOral challengeTranscription factor 6Immune homeostasisCytokine secretionColonic tissueMacrophage functionStress sensorImmune systemRecognition receptorsEffective clearanceMicrobial responsesWeight lossMacrophagesUbiquitination
2014
Cathepsin E Promotes Pulmonary Emphysema via Mitochondrial Fission
Zhang X, Shan P, Homer R, Zhang Y, Petrache I, Mannam P, Lee PJ. Cathepsin E Promotes Pulmonary Emphysema via Mitochondrial Fission. American Journal Of Pathology 2014, 184: 2730-2741. PMID: 25239563, PMCID: PMC4188869, DOI: 10.1016/j.ajpath.2014.06.017.Peer-Reviewed Original ResearchConceptsActivation/apoptosisPulmonary emphysemaChronic obstructive pulmonary disease (COPD) lungsCigarette smoke-induced lung diseaseSmoke-induced lung diseaseChronic obstructive pulmonary diseaseDynamin-related protein 1Obstructive pulmonary diseaseProtein 1Mitochondrial fission protein dynamin-related protein 1Lung tissue sectionsCathepsin ENew therapeutic targetsAir space enlargementFission protein dynamin-related protein 1Pulmonary diseaseEmphysematous changesClinical entityLung diseaseMolecular mechanismsEmphysema developmentMitochondrial fissionLung parenchymaE miceLung elasticity