2023
Investigating rutin as a potential transforming growth factor‐β type I receptor antagonist for the inhibition of bleomycin‐induced lung fibrosis
Karunarathne W, Lee K, Choi Y, Kang C, Lee M, Kim S, Kim G. Investigating rutin as a potential transforming growth factor‐β type I receptor antagonist for the inhibition of bleomycin‐induced lung fibrosis. BioFactors 2023, 50: 477-492. PMID: 38006284, DOI: 10.1002/biof.2020.Peer-Reviewed Original ResearchIdiopathic pulmonary fibrosisEpithelial-mesenchymal transitionPotential of rutinLung fibrosisType I receptor antagonistChronic lung conditionsPotential therapeutic optionTGF-β type I receptorFibrotic signaling pathwaysInhibition of bleomycinSmooth muscle actinNon-toxic concentrationsType I receptorPulmonary fibrosisCancer-related diseasesTherapeutic optionsReceptor antagonistLung conditionsLung fibroblast cellsFibrosisMuscle actinEMT processType 1ECM-related genesTGFAcetate controls endothelial-to-mesenchymal transition
Zhu X, Wang Y, Soaita I, Lee H, Bae H, Boutagy N, Bostwick A, Zhang R, Bowman C, Xu Y, Trefely S, Chen Y, Qin L, Sessa W, Tellides G, Jang C, Snyder N, Yu L, Arany Z, Simons M. Acetate controls endothelial-to-mesenchymal transition. Cell Metabolism 2023, 35: 1163-1178.e10. PMID: 37327791, PMCID: PMC10529701, DOI: 10.1016/j.cmet.2023.05.010.Peer-Reviewed Original ResearchConceptsTGF-β signalingChronic vascular diseaseTGF-β receptor ALK5Mesenchymal transitionInduction of EndMTVascular diseaseMolecular basisPositive feedback loopReceptor ALK5Cellular levelSMADs 2Novel targetEndMT inductionMetabolic modulationMetabolic basisFibrotic stateSignalingPotential treatmentEndMTTGFDiseaseActivationInductionACSS2PDK4Correction: Chitinase 1 regulates pulmonary fibrosis by modulating TGF-β/SMAD7 pathway via TGFBRAP1 and FOXO3
Lee C, He C, Park J, Lee J, Kamle S, Ma B, Akosman B, Cotez R, Chen E, Zhou Y, Herzog E, Ryu C, Peng X, Rosas I, Poli S, Bostwick C, Choi A, Elias J, Lee C. Correction: Chitinase 1 regulates pulmonary fibrosis by modulating TGF-β/SMAD7 pathway via TGFBRAP1 and FOXO3. Life Science Alliance 2023, 6: e202302065. PMID: 37037591, PMCID: PMC10088146, DOI: 10.26508/lsa.202302065.Peer-Reviewed Original Research
2022
Neuronal activity induces glucosylceramide that is secreted via exosomes for lysosomal degradation in glia
Wang L, Lin G, Zuo Z, Li Y, Byeon S, Pandey A, Bellen H. Neuronal activity induces glucosylceramide that is secreted via exosomes for lysosomal degradation in glia. Science Advances 2022, 8: eabn3326. PMID: 35857503, PMCID: PMC9278864, DOI: 10.1126/sciadv.abn3326.Peer-Reviewed Original ResearchEndothelial Cell TGF-β (Transforming Growth Factor-Beta) Signaling Regulates Venous Adaptive Remodeling to Improve Arteriovenous Fistula Patency
Taniguchi R, Ohashi Y, Lee JS, Hu H, Gonzalez L, Zhang W, Langford J, Matsubara Y, Yatsula B, Tellides G, Fahmy TM, Hoshina K, Dardik A. Endothelial Cell TGF-β (Transforming Growth Factor-Beta) Signaling Regulates Venous Adaptive Remodeling to Improve Arteriovenous Fistula Patency. Arteriosclerosis Thrombosis And Vascular Biology 2022, 42: 868-883. PMID: 35510552, PMCID: PMC9233042, DOI: 10.1161/atvbaha.122.317676.Peer-Reviewed Original ResearchConceptsArteriovenous fistulaSMC proliferationAVF patencyCollagen densityMouse aortocaval fistula modelTGF-β receptor IArteriovenous fistula patencyAortocaval fistula modelInhibition of TGFPredetermined time pointsTGF-β inhibitionTGF-β signalingTGF-β receptorDisruption of TGFFistula patencyAVF failureWall thicknessVascular accessVenous remodelingSuccessful hemodialysisDoppler ultrasoundFistula modelReceptor IPatencyTGF
2018
ZEB1, ZEB2, and the miR-200 family form a counterregulatory network to regulate CD8+ T cell fates
Guan T, Dominguez CX, Amezquita RA, Laidlaw BJ, Cheng J, Henao-Mejia J, Williams A, Flavell RA, Lu J, Kaech SM. ZEB1, ZEB2, and the miR-200 family form a counterregulatory network to regulate CD8+ T cell fates. Journal Of Experimental Medicine 2018, 215: 1153-1168. PMID: 29449309, PMCID: PMC5881466, DOI: 10.1084/jem.20171352.Peer-Reviewed Original ResearchConceptsT cellsMemory CD8T cell fateMemory T cell survivalLong-term immunityT cell formationT cell survivalMiR-200 family membersGrowth factor βFamily membersTranscription factor ZEB1Effector CD8MiR-200 familyCD8Mesenchymal transitionReciprocal expression patternCell fateZEB1ZEB2Factor βCell survivalTGFCell formationUnknown genetic pathwaysCell fate decisions
2017
Chapter 7 MicroRNAs in Idiopathic Pulmonary Fibrosis Partners in Health and Disease
Pandit K, Kaminski N. Chapter 7 MicroRNAs in Idiopathic Pulmonary Fibrosis Partners in Health and Disease. 2017, 179-202. DOI: 10.1016/b978-0-12-800553-8.00007-x.Peer-Reviewed Original ResearchIdiopathic pulmonary fibrosisEtiology of IPFInterstitial lung diseaseExtent of fibrosisIPF patientsPulmonary fibrosisIrreversible scarringLung diseaseTreatment optionsAggressive formPotent cytokineGrowth factorDiseaseDreadful diseaseFibrosisLungTGFCurrent knowledgeMicroRNAsTarget genesGas exchangePatientsCytokinesScarringEtiology
2016
Genomic Instability Is Induced by Persistent Proliferation of Cells Undergoing Epithelial-to-Mesenchymal Transition
Comaills V, Kabeche L, Morris R, Buisson R, Yu M, Madden MW, LiCausi JA, Boukhali M, Tajima K, Pan S, Aceto N, Sil S, Zheng Y, Sundaresan T, Yae T, Jordan NV, Miyamoto DT, Ting DT, Ramaswamy S, Haas W, Zou L, Haber DA, Maheswaran S. Genomic Instability Is Induced by Persistent Proliferation of Cells Undergoing Epithelial-to-Mesenchymal Transition. Cell Reports 2016, 17: 2632-2647. PMID: 27926867, PMCID: PMC5320932, DOI: 10.1016/j.celrep.2016.11.022.Peer-Reviewed Original ResearchConceptsGenomic instabilityCancer cellsNuclear envelope proteinsMesenchymal transitionHeritable genetic changesHeritable changesMitotic defectsMitotic regulationTumorigenic phenotypeProliferation arrestMicroenvironment-derived signalsMitotic abnormalitiesStromal signalsGenetic changesMesenchymal marker expressionCancer progressionReversible phenotypeEnvelope proteinEpithelial cellsPersistent proliferationPhenotypeCellsMarker expressionDrug resistanceTGF
2014
Resemble and Inhibit: When RLR Meets TGF-β
Zhu S, Li HB, Flavell RA. Resemble and Inhibit: When RLR Meets TGF-β. Molecular Cell 2014, 56: 719-720. PMID: 25526529, DOI: 10.1016/j.molcel.2014.12.010.Peer-Reviewed Original ResearchLet-7d microRNA affects mesenchymal phenotypic properties of lung fibroblasts
Huleihel L, Ben-Yehudah A, Milosevic J, Yu G, Pandit K, Sakamoto K, Yousef H, LeJeune M, Coon TA, Redinger CJ, Chensny L, Manor E, Schatten G, Kaminski N. Let-7d microRNA affects mesenchymal phenotypic properties of lung fibroblasts. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2014, 306: l534-l542. PMID: 24441869, PMCID: PMC3949080, DOI: 10.1152/ajplung.00149.2013.Peer-Reviewed Original ResearchMeSH KeywordsActinsCadherinsCalcium-Binding ProteinsCell MovementCell ProliferationCells, CulturedEpithelial-Mesenchymal TransitionFibroblastsFibronectinsHMGA2 ProteinHMGB2 ProteinHumansIdiopathic Pulmonary FibrosisKeratin-19LungMicroRNAsMyofibroblastsPulmonary AlveoliPulmonary FibrosisS100 Calcium-Binding Protein A4Snail Family Transcription FactorsTranscription FactorsTransfectionTransforming Growth Factor betaWound HealingZonula Occludens-1 ProteinConceptsLet-7dFibroblast-specific protein-1Mesenchymal marker αProtein 1Tight junction protein 1Smooth muscle actinMicroRNA Let-7dLung fibrosisProliferation of fibroblastsFibrotic processPrimary fibroblastsEffect of transfectionMuscle actinMesenchymal transitionLung fibroblastsFibroblast responsivenessMesenchymal propertiesKeratin 19Protein expressionEpithelial cellsWound healingN-cadherinProtein inductionReduced motilityTGF
2010
Importance of TLR2 in the direct response of T lymphocytes to Schistosoma mansoni antigens
Burton O, Gibbs S, Miller N, Jones F, Wen L, Dunne D, Cooke A, Zaccone P. Importance of TLR2 in the direct response of T lymphocytes to Schistosoma mansoni antigens. European Journal Of Immunology 2010, 40: 2221-2229. PMID: 20480503, DOI: 10.1002/eji.200939998.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDAntigens, HelminthCD4-Positive T-LymphocytesCells, CulturedFemaleForkhead Transcription FactorsGalectin 3Helminth ProteinsHost-Pathogen InteractionsImmunomodulationLectins, C-TypeMiceMice, Inbred C57BLMice, Inbred NODMice, KnockoutMinor Histocompatibility AntigensReceptors, Cell SurfaceSchistosoma mansoniToll-Like Receptor 2Transforming Growth Factor betaConceptsS. mansoni soluble egg antigenSchistosoma mansoni antigensT cellsFoxp3 expressionImportance of TLR2S. mansoni antigensSurface-bound TGFTLR2 ligand stimulationT cell secretionAccessory cell interactionsNOD miceTh2 responsesEgg antigenImmunomodulatory effectsT lymphocytesAbsence of APCC-type lectinBioactive TGFGalectin-3AntigenTGFTLR2Cell interactionsCellsLigand stimulationInterleukin-9 Secretion by Human Th17 Cells is Inducible by TGF-β and Proinflammatory Cytokines and is Increased in Autoimmune Diabetes
Beriou G, Bradshaw E, Lozano E, Baecher-Allan C, Hafler D. Interleukin-9 Secretion by Human Th17 Cells is Inducible by TGF-β and Proinflammatory Cytokines and is Increased in Autoimmune Diabetes. Clinical Immunology 2010, 135: s29. DOI: 10.1016/j.clim.2010.03.089.Peer-Reviewed Original Research
2008
Cross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis
Lin L, Zhou Z, Zheng L, Alber S, Watkins S, Ray P, Kaminski N, Zhang Y, Morse D. Cross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis. American Journal Of Pathology 2008, 173: 337-346. PMID: 18583319, PMCID: PMC2475772, DOI: 10.2353/ajpath.2008.070915.Peer-Reviewed Original ResearchConceptsLung fibrosisPulmonary fibrosisGrowth factorSuppression of fibrosisTranscriptional regulator inhibitorIdiopathic pulmonary fibrosisProgressive lung fibrosisEffects of Id1Activation of TGFInhibited DNA bindingProfibrotic functionsDisease progressionFibrosisFibrotic diseasesDifferentiation 1TGFPotential mechanismsId1FibroblastsNovel binding partnerHuman fibroblastsDRIL1Target genesPatientsLungStructural basis for EGFR ligand sequestration by Argos
Klein DE, Stayrook SE, Shi F, Narayan K, Lemmon MA. Structural basis for EGFR ligand sequestration by Argos. Nature 2008, 453: 1271-1275. PMID: 18500331, PMCID: PMC2526102, DOI: 10.1038/nature06978.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesCell LineCrystallography, X-RayDrosophila melanogasterDrosophila ProteinsEpidermal Growth FactorErbB ReceptorsEye ProteinsHumansLigandsMembrane ProteinsModels, MolecularNerve Tissue ProteinsProtein Structure, TertiaryReceptors, Transforming Growth Factor betaSpodopteraConceptsEpidermal growth factor receptorLigand sequestrationEGFR ligand SpitzLigand SpitzMammalian counterpartsGrowth factor receptorStructural basisUrokinase plasminogen activatorStructural homologuesEGFR ligandsFactor receptorAnticancer therapeuticsStructural resemblanceHomologuesPlasminogen activatorReceptorsSequestrationProteinActivatorLigandsSpitzTGFTherapeuticsDomain
2007
Transforming Growth Factor (TGF)-β1 Stimulates Pulmonary Fibrosis and Inflammation via a Bax-dependent, Bid-activated Pathway That Involves Matrix Metalloproteinase-12*
Kang HR, Cho SJ, Lee CG, Homer RJ, Elias JA. Transforming Growth Factor (TGF)-β1 Stimulates Pulmonary Fibrosis and Inflammation via a Bax-dependent, Bid-activated Pathway That Involves Matrix Metalloproteinase-12*. Journal Of Biological Chemistry 2007, 282: 7723-7732. PMID: 17209037, DOI: 10.1074/jbc.m610764200.Peer-Reviewed Original ResearchConceptsMMP-12Pulmonary fibrosisWild typeGrowth factorInterstitial lung diseaseEffects of TGFMatrix metalloproteinase-12Pulmonary diseaseExaggerated productionPulmonary responseLung diseaseMMP-9Effector functionsTIMP-1Matrix metalloproteinaseFibrosisPotent stimulatorMetalloproteinase-12TGFBax activationInflammationPathogenesisBaxApoptosisDisease
2004
TGF-β1, -β2 and -β3 Cooperate to Facilitate Tubulogenesis in the Explanted Quail Heart
Holifield J, Arlen A, Runyan R, Tomanek R. TGF-β1, -β2 and -β3 Cooperate to Facilitate Tubulogenesis in the Explanted Quail Heart. Journal Of Vascular Research 2004, 41: 491-498. PMID: 15528931, DOI: 10.1159/000081805.Peer-Reviewed Original ResearchConceptsTGF-beta isoformsEndothelial cellsGrowth factor antibodyGrowth factor-beta isoformsEndothelial cell markersFactor antibodyVentricular specimensTGB-betaTGF-β1Angiogenic factorsExogenous TGFCell markersTGFInhibits angiogenesisStimulatory effectGrowth factorInhibitory effectTube formationQuail heartsMarked enhancementAntibodiesVEGFBFGFIsoformsVascular tubesEarly Growth Response Gene 1–mediated Apoptosis Is Essential for Transforming Growth Factor β1–induced Pulmonary Fibrosis
Lee CG, Cho SJ, Kang MJ, Chapoval SP, Lee PJ, Noble PW, Yehualaeshet T, Lu B, Flavell RA, Milbrandt J, Homer RJ, Elias JA. Early Growth Response Gene 1–mediated Apoptosis Is Essential for Transforming Growth Factor β1–induced Pulmonary Fibrosis. Journal Of Experimental Medicine 2004, 200: 377-389. PMID: 15289506, PMCID: PMC2211975, DOI: 10.1084/jem.20040104.Peer-Reviewed Original ResearchConceptsVivo effector functionGrowth factor-β1Early growth response gene-1Pulmonary fibrosisSeptal rupturePulmonary disordersInterstitial diseaseEffector functionsFibrotic responseMurine lungTissue fibrosisEpithelial apoptosisFactor-β1Alveolar remodelingResponse gene-1FibrosisBioactive TGFTGFMyocyte hyperplasiaGrowth factorEarly growth response geneApoptosisLungPathogenesisGene 1Autocrine release of TGF‐β by portal fibroblasts regulates cell growth
Wells RG, Kruglov E, Dranoff JA. Autocrine release of TGF‐β by portal fibroblasts regulates cell growth. FEBS Letters 2004, 559: 107-110. PMID: 14960316, DOI: 10.1016/s0014-5793(04)00037-7.Peer-Reviewed Original ResearchConceptsHepatic stellate cellsPortal fibroblastsBiliary fibrosisGrowth factorTGF-beta2Activated hepatic stellate cellsDerived growth factorTGF-beta receptorsFibroblast growth factorPF proliferationMyofibroblast populationStellate cellsFibrogenic cellsKey growth factorsAutocrine releaseFibrosisCell growthFibroblastsCellsPopulationFactorsTGFLiverReceptors
2003
Loss of integrin αvβ6-mediated TGF-β activation causes Mmp12-dependent emphysema
Morris DG, Huang X, Kaminski N, Wang Y, Shapiro SD, Dolganov G, Glick A, Sheppard D. Loss of integrin αvβ6-mediated TGF-β activation causes Mmp12-dependent emphysema. Nature 2003, 422: 169-173. PMID: 12634787, DOI: 10.1038/nature01413.Peer-Reviewed Original ResearchConceptsTGF-β activationLungs of miceActive TGF-β1Pulmonary gene expressionHeterodimeric cell-surface proteinsTransgenic expressionPulmonary emphysemaMMP12 expressionTGF-β1Functional alterationsΒ6 integrinIntegrin αvβ6Latent TGFMarked inductionEmphysemaGrowth factorMacrophage metalloelastaseCell surface proteinsActivation pathwayMiceTGFActivationCell growthIntegrinsExpression
2002
Immunosuppresive Factors in Cancer
Bucala R, Metz C. Immunosuppresive Factors in Cancer. 2002, 119-154. DOI: 10.1002/3527600795.ch7.Peer-Reviewed Original Research
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