2018
Reducing protein oxidation reverses lung fibrosis
Anathy V, Lahue KG, Chapman DG, Chia SB, Casey DT, Aboushousha R, van der Velden JLJ, Elko E, Hoffman SM, McMillan DH, Jones JT, Nolin JD, Abdalla S, Schneider R, Seward DJ, Roberson EC, Liptak MD, Cousins ME, Butnor KJ, Taatjes DJ, Budd RC, Irvin CG, Ho YS, Hakem R, Brown KK, Matsui R, Bachschmid MM, Gomez JL, Kaminski N, van der Vliet A, Janssen-Heininger YMW. Reducing protein oxidation reverses lung fibrosis. Nature Medicine 2018, 24: 1128-1135. PMID: 29988126, PMCID: PMC6204256, DOI: 10.1038/s41591-018-0090-y.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisLung fibrosisDirect administrationAirways of miceGrowth factor beta 1Transgenic mouse modelFibrotic lungsLung tissueMouse modelAged animalsFibrosisLung epitheliumTherapeutic potentialExcessive depositionBeta 1Transgenic overexpressionOxidative stressExact mechanismAirwayGlrxLungMiceAdministrationOxidative mechanisms
2014
Cholesterol Sulfate and Cholesterol Sulfotransferase Inhibit Gluconeogenesis by Targeting Hepatocyte Nuclear Factor 4α
Shi X, Cheng Q, Xu L, Yan J, Jiang M, He J, Xu M, Stefanovic-Racic M, Sipula I, O'Doherty RM, Ren S, Xie W. Cholesterol Sulfate and Cholesterol Sulfotransferase Inhibit Gluconeogenesis by Targeting Hepatocyte Nuclear Factor 4α. Molecular And Cellular Biology 2014, 34: 485-497. PMID: 24277929, PMCID: PMC3911511, DOI: 10.1128/mcb.01094-13.Peer-Reviewed Original ResearchMeSH KeywordsAcetylationAnimalsBlotting, WesternCarcinoma, HepatocellularCell Line, TumorCell NucleusCells, CulturedCholesterol EstersCoenzyme A LigasesColforsinDiet, High-FatGene ExpressionGluconeogenesisGlucoseHepatocyte Nuclear Factor 4HumansInsulin ResistanceMiceMice, Inbred C57BLMice, ObeseMice, TransgenicObesityReverse Transcriptase Polymerase Chain ReactionSulfotransferasesConceptsDiet-induced obesityHepatocyte nuclear factor 4αNuclear factor 4αCholesterol sulfateLeptin-deficient miceTreatment of micePotential therapeutic targetPotential therapeutic agentExpression of SULT2B1bMetabolic abnormalitiesObese miceMetabolic disordersImportant metabolic regulatorGlucose metabolismTherapeutic targetTransgenic miceFed stateHepatic gluconeogenesisTherapeutic agentsMiceTransgenic overexpressionSULT2B1bMetabolic regulatorFunctional homeostasisInhibits gluconeogenesis
2013
miR-17∼92 miRNA cluster promotes kidney cyst growth in polycystic kidney disease
Patel V, Williams D, Hajarnis S, Hunter R, Pontoglio M, Somlo S, Igarashi P. miR-17∼92 miRNA cluster promotes kidney cyst growth in polycystic kidney disease. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: 10765-10770. PMID: 23759744, PMCID: PMC3696812, DOI: 10.1073/pnas.1301693110.Peer-Reviewed Original ResearchConceptsMiRNA clusterKidney cyst growthPolycystic kidney diseasePosttranscriptional gene expressionCyst growthOncogenic miRNA clusterShort noncoding RNAsKidney-specific inactivationKidney cyst formationDysregulated miRNA expressionPosttranscriptional repressionNoncoding RNAsHyperproliferative epithelial cellsGene dosageGene expressionHepatocyte nuclear factor-1βGenes PKD1Common genetic causeMiRNA expressionMouse modelFluid-filled cystsMiRNAsKidney diseaseTransgenic overexpressionKidney cysts
2007
P21 Regulates TGF-β1–Induced Pulmonary Responses via a TNF-α–Signaling Pathway
Yamasaki M, Kang HR, Homer RJ, Chapoval SP, Cho SJ, Lee BJ, Elias JA, Lee CG. P21 Regulates TGF-β1–Induced Pulmonary Responses via a TNF-α–Signaling Pathway. American Journal Of Respiratory Cell And Molecular Biology 2007, 38: 346-353. PMID: 17932374, PMCID: PMC2258454, DOI: 10.1165/rcmb.2007-0276oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCrosses, GeneticCyclin-Dependent Kinase Inhibitor p21DoxycyclineFibrosisImmunohistochemistryInflammationLungMiceMice, Inbred C57BLMice, TransgenicRandom AllocationRNA, MessengerSignal TransductionStatistics as TopicTransforming Growth Factor beta1Tumor Necrosis Factor-alphaConceptsMurine lungCyclin-dependent kinase inhibitorAbsence of p21Caspase-3 activationP21 locusKey regulatorTNF-alpha expressionEffects of TGFExpression of p21Negative modulatorAlveolar destructionLung inflammationTransgenic overexpressionParenchymal destructionPulmonary responseApoptosisRepair responseP21 expressionRegulatory cytokinesMyofibroblast accumulationP21TGF-β1Epithelial cellsEpithelial apoptosisKinase inhibitors
2002
Transgenic Overexpression of Interleukin (IL)-10 in the Lung Causes Mucus Metaplasia, Tissue Inflammation, and Airway Remodeling via IL-13-dependent and -independent Pathways*
Lee CG, Homer RJ, Cohn L, Link H, Jung S, Craft JE, Graham BS, Johnson TR, Elias JA. Transgenic Overexpression of Interleukin (IL)-10 in the Lung Causes Mucus Metaplasia, Tissue Inflammation, and Airway Remodeling via IL-13-dependent and -independent Pathways*. Journal Of Biological Chemistry 2002, 277: 35466-35474. PMID: 12107190, DOI: 10.1074/jbc.m206395200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceChloride ChannelsCloning, MolecularDNA PrimersFluorescent Antibody TechniqueGene Expression RegulationIn Situ HybridizationInflammationInterleukin-10Interleukin-13LungMiceMice, TransgenicMolecular Sequence DataMucoproteinsMucous MembranePhenotypePolymerase Chain ReactionReceptors, Interleukin-4STAT6 Transcription FactorTrans-ActivatorsConceptsMucus metaplasiaIL-10Tissue inflammationIL-13Tumor necrosis factor productionIL-13/ILLipopolysaccharide-induced inflammationNecrosis factor productionAirway fibrosisNeutrophil accumulationAirway remodelingSubepithelial fibrosisGob-5Levels of mRNAMetaplasiaInflammationTransgenic miceFibrosisSTAT-6Effector propertiesTransgenic overexpressionFactor productionMiceInterleukinMultiple mechanisms
1999
Parathyroid hormone-related protein signaling is necessary for sexual dimorphism during embryonic mammary development
Dunbar M, Dann P, Robinson G, Hennighausen L, Zhang J, Wysolmerski J. Parathyroid hormone-related protein signaling is necessary for sexual dimorphism during embryonic mammary development. Development 1999, 126: 3485-3493. PMID: 10409496, DOI: 10.1242/dev.126.16.3485.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, Genetically ModifiedApoptosisEpithelial CellsFemaleGene Expression Regulation, DevelopmentalHeterozygoteMaleMammary Glands, AnimalMesodermMiceMice, KnockoutParathyroid Hormone-Related ProteinProteinsReceptor, Parathyroid Hormone, Type 1Receptors, AndrogenReceptors, Parathyroid HormoneSex CharacteristicsTenascinConceptsAndrogen receptorMammary mesenchymeMammary budPTH/PTHrP receptorParathyroid hormone-related proteinHormone-related proteinEpithelial budsAR expressionPTHrP expressionMale micePTHrP receptorEmbryonic mammary developmentMammary epithelial cellsEpithelial-mesenchymal signalingMammary developmentTransgenic overexpressionMammary glandBasal epidermisEpithelial cellsC expressionTenascin CVentral dermisReceptorsAndrogensPTHrP
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