2018
Surfactant protein C dampens inflammation by decreasing JAK/STAT activation during lung repair
Jin H, Ciechanowicz AK, Kaplan AR, Wang L, Zhang P, Lu YC, Tobin RE, Tobin BA, Cohn L, Zeiss CJ, Lee PJ, Bruscia EM, Krause DS. Surfactant protein C dampens inflammation by decreasing JAK/STAT activation during lung repair. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2018, 314: l882-l892. PMID: 29345196, PMCID: PMC6008135, DOI: 10.1152/ajplung.00418.2017.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDisease Models, AnimalIntercellular Signaling Peptides and ProteinsJanus Kinase 1Lung InjuryMiceMice, Inbred C57BLMice, KnockoutPeptidesPhosphorylationPneumoniaPulmonary Surfactant-Associated Protein CSTAT3 Transcription FactorThymidine KinaseConceptsAcute respiratory distress syndromeKO miceSurfactant protein CClinical acute respiratory distress syndromeProtein CAlveolar type 2 cellsAnti-inflammatory mediatorsRespiratory distress syndromeBronchoalveolar lavage fluidAnti-inflammatory moleculesPhosphorylated signal transductionType 2 cellsSPC expressionInducible suicide geneJanus kinaseLevels of suppressorDistress syndromeBAL fluidGranulocyte infiltrationJAK1/2 inhibitorLavage fluidProinflammatory phenotypeInflammatory cytokinesSevere inflammationInjury model
2016
The Wnt Antagonist Dickkopf-1 Promotes Pathological Type 2 Cell-Mediated Inflammation
Chae WJ, Ehrlich AK, Chan PY, Teixeira AM, Henegariu O, Hao L, Shin JH, Park JH, Tang WH, Kim ST, Maher SE, Goldsmith-Pestana K, Shan P, Hwa J, Lee PJ, Krause DS, Rothlin CV, McMahon-Pratt D, Bothwell AL. The Wnt Antagonist Dickkopf-1 Promotes Pathological Type 2 Cell-Mediated Inflammation. Immunity 2016, 44: 246-258. PMID: 26872695, PMCID: PMC4758884, DOI: 10.1016/j.immuni.2016.01.008.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, DermatophagoidesAntigens, ProtozoanAsthmaBlood PlateletsCell DifferentiationCells, CulturedCytokinesExtracellular Signal-Regulated MAP KinasesGene Expression RegulationHumansInflammationIntercellular Signaling Peptides and ProteinsLeishmania majorLeishmaniasis, CutaneousMiceMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicModels, AnimalPyroglyphidaeSignal TransductionTh2 CellsTOR Serine-Threonine KinasesWnt ProteinsConceptsCell-mediated inflammationTh2 cell cytokine productionCell cytokine productionLeukocyte-platelet aggregatesLeukocyte infiltrationDkk-1Cytokine productionT helper 2 cellsLeishmania major infectionHouse dust miteTranscription factor c-MafAllergen challengeMajor infectionDust miteImmune responseDickkopf-1Parasitic infectionsGATA-3Pathological roleFunctional inhibitionInflammationC-MafP38 MAPKInfiltrationInfection
2011
Increased Tubular Proliferation as an Adaptive Response to Glomerular Albuminuria
Guo JK, Marlier A, Shi H, Shan A, Ardito TA, Du ZP, Kashgarian M, Krause DS, Biemesderfer D, Cantley LG. Increased Tubular Proliferation as an Adaptive Response to Glomerular Albuminuria. Journal Of The American Society Of Nephrology 2011, 23: 429-437. PMID: 22193389, PMCID: PMC3294312, DOI: 10.1681/asn.2011040396.Peer-Reviewed Original ResearchMeSH KeywordsAlbuminuriaAnimalsAxl Receptor Tyrosine KinaseCell ProliferationDisease Models, AnimalFemaleHeparin-binding EGF-like Growth FactorIntegrasesIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsKidney GlomerulusKidney Tubules, ProximalMaleMembrane ProteinsMiceMice, TransgenicPodocytesProteinuriaProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesConceptsGlomerular proteinuriaTubular injuryTubular proliferationStructural glomerular injuryProteinuric renal diseaseOnset of albuminuriaRenal tubular atrophyDiphtheria toxin receptorRenal tubular cellsProximal tubule cellsGlomerular albuminuriaRenal failureSystemic inflammationTubular damageProgressive glomerulosclerosisRenal diseaseTubular atrophyGlomerular injuryRenal responsePodocyte lossProliferative responseTubular cellsAnimal modelsProteinuriaReceptor Axl
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