2023
α1 Adrenoreceptor antagonism mitigates extracellular mitochondrial DNA accumulation in lung fibrosis models and in patients with idiopathic pulmonary fibrosis
Ishikawa G, Peng X, McGovern J, Woo S, Perry C, Liu A, Yu S, Ghincea A, Kishchanka A, Fiorini V, Hu B, Sun Y, Sun H, Ryu C, Herzog E. α1 Adrenoreceptor antagonism mitigates extracellular mitochondrial DNA accumulation in lung fibrosis models and in patients with idiopathic pulmonary fibrosis. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2023, 324: l639-l651. PMID: 36648147, PMCID: PMC10110730, DOI: 10.1152/ajplung.00119.2022.Peer-Reviewed Original ResearchConceptsAdrenergic nerve supplyIdiopathic pulmonary fibrosisΑ1 adrenoreceptorsPulmonary fibrosisNerve supplyCultured normal human lung fibroblastsInnate immune ligandsLung fibrosis modelNormal human lung fibroblastsSmooth muscle actinHuman lung fibroblastsAdrenal resectionAdrenoreceptor antagonismExtracellular mtDNAIPF cohortImproved survivalΑ1-adrenoreceptor antagonistsLung fibrosisAdrenal sourceFibroblast accumulationAdrenoreceptor antagonistBleomycin modelFibrosis modelLung fibrogenesisMouse modelIFN-γ Is Protective in Cytokine Release Syndrome-associated Extrapulmonary Acute Lung Injury.
Sun Y, Hu B, Stanley G, Harris ZM, Gautam S, Homer R, Koff JL, Rajagopalan G. IFN-γ Is Protective in Cytokine Release Syndrome-associated Extrapulmonary Acute Lung Injury. American Journal Of Respiratory Cell And Molecular Biology 2023, 68: 75-89. PMID: 36125351, PMCID: PMC9817908, DOI: 10.1165/rcmb.2022-0117oc.Peer-Reviewed Original ResearchConceptsCytokine release syndromeAcute lung injuryExtrapulmonary acute lung injuryIFN-γ KO miceIL-17ALung injuryKO miceStaphylococcal enterotoxin BRelease syndromeIL-17A KO miceSevere acute lung injuryAcute respiratory distress syndromeSystemic T cell activationEnterotoxin BAdaptive T lymphocytesDR3 transgenic miceNeutralization of IFNRespiratory distress syndromeHuman leukocyte antigenRole of IFNT cell cytokinesJanus kinase inhibitorS100A8/A9T cell activationALI parameters
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
2017
Lung Endothelial MicroRNA-1 Regulates Tumor Growth and Angiogenesis
Korde A, Jin L, Zhang JG, Ramaswamy A, Hu B, Kolahian S, Guardela BJ, Herazo-Maya J, Siegfried JM, Stabile L, Pisani MA, Herbst RS, Kaminski N, Elias JA, Puchalski JT, Takyar SS. Lung Endothelial MicroRNA-1 Regulates Tumor Growth and Angiogenesis. American Journal Of Respiratory And Critical Care Medicine 2017, 196: 1443-1455. PMID: 28853613, PMCID: PMC5736970, DOI: 10.1164/rccm.201610-2157oc.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerMiR-1 levelsLewis lung carcinoma xenograftsLung carcinoma xenograftsTransgenic miceEndothelial cellsNSCLC tumorsCarcinoma xenograftsLung endotheliumMiR-1Tumor growthTumor progressionVascular endothelial cadherin promoterMicroRNA-1Cohort of patientsTumor-bearing lungsCell lung cancerVascular endothelial growth factorCancer-free tissuesEndothelial growth factorInducible transgenic miceMiR-1 overexpressionKP miceOverall survivalTumor burden
2014
Chitinase 3–Like 1 Suppresses Injury and Promotes Fibroproliferative Responses in Mammalian Lung Fibrosis
Zhou Y, Peng H, Sun H, Peng X, Tang C, Gan Y, Chen X, Mathur A, Hu B, Slade MD, Montgomery RR, Shaw AC, Homer RJ, White ES, Lee CM, Moore MW, Gulati M, Lee CG, Elias JA, Herzog EL. Chitinase 3–Like 1 Suppresses Injury and Promotes Fibroproliferative Responses in Mammalian Lung Fibrosis. Science Translational Medicine 2014, 6: 240ra76. PMID: 24920662, PMCID: PMC4340473, DOI: 10.1126/scitranslmed.3007096.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisCHI3L1 levelsChitinase 3Lungs of patientsAlternative macrophage activationLevel of apoptosisAcute exacerbationFibroproliferative repairLung transplantationDisease exacerbationInjury phaseAmbulatory patientsEpithelial injuryPulmonary fibrosisIPF populationLung fibrosisMacrophage accumulationCHI3L1 expressionFibrotic phaseDisease progressionProfibrotic roleFibroproliferative responseMacrophage activationMyofibroblast transformationProtective role
2008
IL-13 Receptor α2 Selectively Inhibits IL-13-Induced Responses in the Murine Lung
Zheng T, Liu W, Oh SY, Zhu Z, Hu B, Homer RJ, Cohn L, Grusby MJ, Elias JA. IL-13 Receptor α2 Selectively Inhibits IL-13-Induced Responses in the Murine Lung. The Journal Of Immunology 2008, 180: 522-529. PMID: 18097054, DOI: 10.4049/jimmunol.180.1.522.Peer-Reviewed Original ResearchConceptsIL-13Ralpha2Pulmonary inflammationIL-13Inflammatory responseMurine lungHigh-affinity IL-13 receptorsTransgenic IL-13IL-13 receptor α2Production of chemokinesEnhanced inflammatory responseIL-13 receptorMucus metaplasiaTh2 inflammationAirway remodelingSubepithelial fibrosisIL-4Receptor α2Critical cytokineIL-13Ralpha1IL-4RalphaDecoy receptorPhysiologic responsesInflammationTissue effectsReceptors
2007
Lung‐specific nuclear reprogramming is accompanied by heterokaryon formation and Y chromosome loss following bone marrow transplantation and secondary inflammation
Herzog EL, Van Arnam J, Hu B, Zhang J, Chen Q, Haberman AM, Krause DS. Lung‐specific nuclear reprogramming is accompanied by heterokaryon formation and Y chromosome loss following bone marrow transplantation and secondary inflammation. The FASEB Journal 2007, 21: 2592-2601. PMID: 17449722, DOI: 10.1096/fj.06-7861com.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow TransplantationChromosome DeletionFemaleInflammationIntercellular Signaling Peptides and ProteinsMaleMiceMice, KnockoutPeptidesPostoperative ComplicationsPulmonary Surfactant-Associated Protein CTransplantation ChimeraTransplantation ConditioningWhole-Body IrradiationY ChromosomeConceptsTransplanted bone marrow-derived cellsY chromosomeHeterokaryon formationBone marrow-derived cellsLung-specific gene expressionGene expression patternsSurfactant protein CY chromosome lossNuclear reprogrammingSP-C mRNAChromosome lossExpression patternsGene expressionCell fusionSP-C deficiencyChromosomesReprogrammingSpNonhematopoietic cellsWild-type marrowMarrow-derived cellsCellsProtein CProteinFusion
2006
Threshold of Lung Injury Required for the Appearance of Marrow‐Derived Lung Epithelia
Herzog EL, Van Arnam J, Hu B, Krause DS. Threshold of Lung Injury Required for the Appearance of Marrow‐Derived Lung Epithelia. Stem Cells 2006, 24: 1986-1992. PMID: 16868209, DOI: 10.1634/stemcells.2005-0579.Peer-Reviewed Original ResearchConceptsBone marrow-derived cellsBone marrow transplantationLung injuryMarrow transplantationLung epitheliumEngraftment of BMDCsLocal host factorsSex-mismatched bone marrow transplantationMarrow-derived cellsType II pneumocytesMyeloablative radiationLung damageHematopoietic chimerismEpithelial chimerismApparent injuryInjuryTransplantationHost factorsEpitheliumEpithelial cellsEpithelial phenotypeLungChimerismPneumocytesPhenotypic changes