Search results for "Transforming growth factor"

showing 10 items of 294 documents

Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms

2021

Interstitial lung diseases (ILDs) comprise different fibrotic lung disorders characterized by cellular proliferation, interstitial inflammation, and fibrosis. The JAK/STAT molecular pathway is activated under the interaction of a broad number of profibrotic/pro-inflammatory cytokines, such as IL-6, IL-11, and IL-13, among others, which are increased in different ILDs. Similarly, several growth factors over-expressed in ILDs, such as platelet-derived growth factor (PDGF), transforming growth factor β1 (TGF-β1), and fibroblast growth factor (FGF) activate JAK/STAT by canonical or non-canonical pathways, which indicates a predominant role of JAK/STAT in ILDs. Between the different JAK/STAT iso…

QH301-705.5medicine.medical_treatmentReviewCatalysisstatInorganic ChemistryPulmonary fibrosismedicineHumansProtein IsoformsPhysical and Theoretical ChemistryBiology (General)STAT3Molecular BiologyProtein Kinase InhibitorsQD1-999SpectroscopyCellular SenescenceJanus KinasesbiologyChemistryGrowth factorInterleukinsinterstitial lung disease (ILD)Organic ChemistryJAK-STAT signaling pathwayGeneral Medicinerespiratory systemmedicine.diseaseEndoplasmic Reticulum StressComputer Science Applicationsrespiratory tract diseasesSTAT Transcription FactorsChemistrysignal transducer and activator of transcription (STAT)biology.proteinCancer researchidiopathic pulmonary fibrosis (IPF)Janus kinaseLung Diseases InterstitialJanus kinases (JAK)Platelet-derived growth factor receptorTransforming growth factorSignal TransductionInternational Journal of Molecular Sciences
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Pre- and Post-translational Regulation of Lysyl Oxidase by Transforming Growth Factor-β1 in Osteoblastic MC3T3-E1 Cells

1995

The final enzymatic step required for collagen cross-linking is the extracellular oxidative deamination of peptidyl-lysine and -hydroxylysine residues by lysyl oxidase. A cross-linked collagenous extracellular matrix is required for bone formation. The goals of this study were to compare the transforming growth factor (TGF)-beta 1 regulation of lysyl oxidase enzyme activity and steady state mRNA levels to changes in COL1A1 mRNA levels in MC3T3-E1 osteoblastic cells. TGF-beta 1 increased steady state lysyl oxidase and COL1A1 mRNA levels in a dose- and time-dependent manner. The increase in lysyl oxidase mRNA levels was transient, peaking at 12 h and 8.8 times controls in cells treated with 4…

Recombinant Fusion ProteinsLysyl oxidasemacromolecular substancesBiochemistryGene Expression Regulation EnzymologicProtein-Lysine 6-OxidaseExtracellular matrixMicechemistry.chemical_compoundTransforming Growth Factor betaEndopeptidasesTranslational regulationExtracellularAnimalsHumansRNA Messengerskin and connective tissue diseasesMolecular BiologyOsteoblastsintegumentary systembiologyOxidative deamination3T3 CellsCell BiologyMolecular biologyRecombinant ProteinsEnzyme assayKineticsHydroxylysinechemistrybiology.proteinElectrophoresis Polyacrylamide GelCollagenProtein Processing Post-TranslationalTransforming growth factorJournal of Biological Chemistry
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Les IAP au cœur de la signalisation NF-κB

2012

The function of IAP has long been limited to an inhibition of apoptosis through their capacity to bind some caspases. Since the expression of these proteins is altered in some tumor samples, IAPs are targets for anticancer therapy and many small molecules have been designed for their capacity to inhibit IAP-caspase interaction. Unexpectedly, these molecules appeared to significantly affect NF-κB activation. In this review, we will discuss the central role of cIAP1, cIAP2 and XIAP in the regulation of NF-κB activating signaling pathways.

Regulation of gene expressionbiologyGeneral MedicineTransforming growth factor betaNFKB1General Biochemistry Genetics and Molecular BiologyCell biologyXIAPbody regionsApoptosisImmunologybiology.proteinSignal transductionReceptorCaspasemédecine/sciences
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Cutting Edge: Trans-Signaling via the Soluble IL-6R Abrogates the Induction of FoxP3 in Naive CD4+CD25− T Cells

2007

Abstract Chronic inflammatory diseases may develop when regulatory T cells (Tregs) fail to control the balance between tolerance and immunity. Alternatively, activated immune cells might prevent the induction or activation of Tregs in such diseases. In this study, we demonstrate that trans-signaling into T cells via the soluble IL-6 receptor completely abrogates the de novo induction of adaptive Tregs. Mechanistically, IL-6 trans-signaling augmented the expression of the TGF-β signaling inhibitor SMAD7. Consequently, SMAD7 overexpression in T cells using newly created transgenic mice rendered CD4+CD25− T cells resistant to the induction of FoxP3. Finally, IL-6 trans-signaling inhibited Treg…

Regulatory T cellImmunologyMice Transgenicchemical and pharmacologic phenomenaMice SCIDBiologyT-Lymphocytes RegulatoryAutoimmune DiseasesSmad7 ProteinMiceInterleukin 21Immune systemTransforming Growth Factor betaImmunitymedicineAnimalsHumansImmunology and AllergyCytotoxic T cellIL-2 receptorInflammationMice Inbred BALB CInterleukin-6ZAP70FOXP3Forkhead Transcription FactorsColitisReceptors Interleukin-6Cell biologyDisease Models Animalmedicine.anatomical_structureGene Expression RegulationChronic DiseaseImmunologySignal TransductionThe Journal of Immunology
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Tumor cells convert immature myeloid dendritic cells into TGF-β–secreting cells inducing CD4+CD25+ regulatory T cell proliferation

2005

The mechanisms through which regulatory T cells accumulate in lymphoid organs of tumor-bearing hosts remain elusive. Our experiments indicate that the accumulation of CD4+CD25+ regulatory T cells (T reg cells) expressing FoxP3 and exhibiting immunosuppressive function originates from the proliferation of naturally occurring CD25+ T cells and requires signaling through transforming growth factor (TGF)–β receptor II. During tumor progression, a subset of dendritic cells (DCs) exhibiting a myeloid immature phenotype is recruited to draining lymph nodes. This DC subset selectively promotes the proliferation of T reg cells in a TGF-β–dependent manner in mice and rats. Tumor cells are necessary a…

Regulatory T cellImmunologychemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryArticleMiceInterleukin 21Transforming Growth Factor betaCell Line TumorNeoplasmsmedicineAnimalsImmunology and AllergyCytotoxic T cellIL-2 receptorAntigen-presenting cellCell ProliferationDNA PrimersInterleukin 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationForkhead Transcription FactorsRats Inbred Strainshemic and immune systemsDendritic CellsNatural killer T cellImmunohistochemistryMolecular biologyRatsCell biologymedicine.anatomical_structureBromodeoxyuridineInterleukin 12Receptors Transforming Growth Factor betaSignal TransductionJournal of Experimental Medicine
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Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes.

2020

Background: Naturally occurring variation in Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), encoding for an enzyme involved in phosphatidylinositol acyl-chain remodelling, has been associated with fatty liver and hepatic disorders. Here, we examined the relationship between hepatic Mboat7 down-regulation and fat accumulation. Methods: Hepatic MBOAT7 expression was surveyed in 119 obese individuals and in experimental models. MBOAT7 was acutely silenced by antisense oligonucleotides in C57Bl/6 mice, and by CRISPR/Cas9 in HepG2 hepatocytes. Findings: In obese individuals, hepatic MBOAT7 mRNA decreased from normal liver to steatohepatitis, independently of diabetes, inflammatio…

Research paperTGFβ Transforming Growth Factor BetaIntracellular SpaceCRISPR Clustered Regularly Interspaced Short Palindromic RepeatshHEPS Human HepatocytesMice0302 clinical medicineLPIAT1DAG Diacylglyceroli.p. Intraperitonealmedia_commonFatty AcidsGeneral Medicine3. Good health030220 oncology & carcinogenesisHOMA-IR homeostasis Model Assessment of Insulin ResistanceMPO morpholinolcsh:Medicine (General)medicine.medical_specialtyPE Phosphatidyl-EthanolamineNashGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesTNFα tumor Necrosis Factor AlphaLDL Low Density LipoproteinsHyperinsulinismNAFLDSD Standard Dietmedia_common.cataloged_instanceHumansCPT1 Carnitine Palmitoyltransferase IPhosphatidylinositolGene SilencingEuropean unionVLDL Very Low Density Lipoproteinlcsh:RhHSC Human Hepatic Stellate Cellsmedicine.diseaseLipid MetabolismOA Oleic AcidCI Confidence IntervalMboat7 Membrane bound O-acyltransferase domain containing 7MCD methionine choline deficient diet030104 developmental biologyEndocrinologychemistryCDP Cytidine-DiphosphateFOXO1 Forkhead Box protein O1NAFLD nonalcoholic fatty liver diseaseSteatohepatitisBMI Body Mass IndexCL CardiolipinAcyltransferases0301 basic medicineAlcoholic liver diseaseCXCL10 C-X-C Motif Chemokine 10lcsh:Medicinechemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseIFG Impaired Fasting GlucoseAPOB Apolipoprotein BNonalcoholic fatty liver diseasePIP Phosphatidyl-Inositol-PhosphateSteatohepatitisqRT-PCR quantitative Real Time Polymerase Chain ReactionMice Knockoutlcsh:R5-920ORO Oil Red O StainingPI PhosphatidylinositolFatty liverTM6SF2 Transmembrane 6 Superfamily Member 2PhospholipidTAG TriglyceridesNASH Nonalcoholic SteatohepatitisLipogenesisLPA Lyso-Phosphatidic AcidPhosphatidylinositolSignal TransductionPS Phosphatidyl-SerinePA Palmitic AcidALD alcoholic liver diseasePC Phosphatidylcholinei.v. IntravenousFATP1 Fatty Acid Transport Protein 1Models BiologicalInternal medicinemedicineAnimalsNonalcoholic fatty liver diseasePPARα Peroxisome Proliferator-Activated Receptor alphaObesityG3P Glyceraldehyde-3-PhosphateSREBP1c Sterol Regulatory Element-Binding Protein 1HDL High Density Lipoproteinsbusiness.industryPI3K Phosphatidylinositol 3 KinaseMembrane ProteinsNHEJ Non-Homologues End JoiningPNPLA3 Patatin-like Phospholipase Domain-containing-3MTTP Microsomal Triglyceride Transfer ProteinLPIAT1 Lysophosphatidylinositol Acyltransferase 1TMC4 Transmembrane Channel-Like 4Disease Models AnimalGene Expression RegulationHepatocytesFOXA2 Forkhead Box A2mTOR mammalian target of RapamycinSteatosisInsulin ResistancebusinessPG Phosphatidyl-GlycerolFABP1 Fatty Acid-Binding Protein 1 FAS Fatty Acid SynthaseT2DM Type 2 Diabetes MellitusEBioMedicine
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GAM/ZFp/ZNF512B is central to a gene sensor circuitry involving cell-cycle regulators, TGF beta effectors, Drosha and microRNAs with opposite oncogen…

2010

MicroRNAs (miRNAs) are small regulatory RNAs targeting multiple effectors of cell homeostasis and development, whose malfunctions are associated with major pathologies such as cancer. Herein we show that GAM/ZFp/ZNF512B works within an intricate gene regulatory network involving cell-cycle regulators, TGFβ effectors and oncogenic miRNAs of the miR-17-92 cluster. Thus, GAM impairs the transcriptional activation of the miR-17-92 promoter by c-Myc, downregulates miR-17-92 miRNAs differentially, and limits the activation of genes responsive to TGFβ canonical pathway. In contrast, TGFβ decreases GAM transcripts levels while differentially upregulating miR-17-92 miRNAs. In turn, miR-17, miR-20a a…

Ribonuclease IIITranscriptional ActivationRegulatorGene regulatory networkBiologyProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)Transforming Growth Factor betamicroRNAGeneticsE2F1HumansGene Regulatory NetworksDroshaFeedback PhysiologicalEffectorCell CycleTransforming growth factor betaCell cycleCell biologyMicroRNAsbiology.proteinCancer researchRNACarrier ProteinsE2F1 Transcription Factor
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Increased serum miR-193a-5p during non-alcoholic fatty liver disease progression: Diagnostic and mechanistic relevance

2022

Background & Aims Serum microRNA (miRNA) levels are known to change in non-alcoholic fatty liver disease (NAFLD) and may serve as useful biomarkers. This study aimed to profile miRNAs comprehensively at all NAFLD stages. Methods We profiled 2,083 serum miRNAs in a discovery cohort (183 cases with NAFLD representing the complete NAFLD spectrum and 10 population controls). miRNA libraries generated by HTG EdgeSeq were sequenced by Illumina NextSeq. Selected serum miRNAs were profiled in 372 additional cases with NAFLD and 15 population controls by quantitative reverse transcriptase PCR. Results Levels of 275 miRNAs differed between cases and population controls. Fewer differences were seen wi…

SCORING SYSTEMCPM counts per millionAUROC area under the receiver operating characteristicRC799-869AST aspartate aminotransferaseMicroRNA; Non-alcoholic fatty liver disease; Biomarker; SequencingTGF-β transforming growth factor-betaGastroenterologySTEATOHEPATITISLiver disease0302 clinical medicineFibrosismiRNA microRNAlogFC log2 fold changeFIBROSISImmunology and AllergySequencing0303 health scienceseducation.field_of_studyNAS NAFLD activity scoremedicine.diagnostic_testFatty liverGastroenterologyGTEx Genotype-Tissue ExpressionMicroRNADiseases of the digestive system. Gastroenterology3. Good healthReal-time polymerase chain reactionBiomarker MicroRNA Non-alcoholic fatty liver disease SequencingLiver biopsyACIDBiomarker (medicine)030211 gastroenterology & hepatologyLife Sciences & BiomedicineResearch ArticleEXPRESSIONmedicine.medical_specialtyNAFLD non-alcoholic fatty liver diseaseNASH non-alcoholic steatohepatitisPopulationGastroenterology and HepatologySAF steatosis–activity–fibrosisVALIDATIONER endoplasmic reticulum03 medical and health sciencescDNA complementary DNAInternal medicineALT alanine aminotransferaseGastroenterologiInternal MedicinemedicineNAFL non-alcoholic fatty liverALGORITHMFIB-4 fibrosis-4education030304 developmental biologyPCA principal component analysisScience & TechnologyGastroenterology & HepatologyHepatologybusiness.industryBiomarkerFC fold changemedicine.diseaseBiomarker; MicroRNA; Non-alcoholic fatty liver disease; Sequencingdigestive system diseasesFLIP fatty liver inhibition of progressionCt cycle thresholdSteatosisqPCR quantitative PCRbusinessNon-alcoholic fatty liver disease
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Generation of T Follicular Helper Cells Is Mediated by Interleukin-21 but Independent of T Helper 1, 2, or 17 Cell Lineages

2008

After activation, CD4(+) helper T (Th) cells differentiate into distinct effector subsets. Although chemokine (C-X-C motif) receptor 5-expressing T follicular helper (Tfh) cells are important in humoral immunity, their developmental regulation is unclear. Here we show that Tfh cells had a distinct gene expression profile and developed in vivo independently of the Th1 or Th2 cell lineages. Tfh cell generation was regulated by ICOS ligand (ICOSL) expressed on B cells and was dependent on interleukin-21 (IL-21), IL-6, and signal transducer and activator of transcription 3 (STAT3). However, unlike Th17 cells, differentiation of Tfh cells did not require transforming growth factor beta (TGF-beta…

STAT3 Transcription FactorAdoptive cell transferCellular differentiationCellImmunologyGene ExpressionLymphocyte ActivationCXCR5ArticleInducible T-Cell Co-Stimulator LigandMiceInterleukin 21T-Lymphocyte SubsetsTransforming Growth Factor betaFollicular phasemedicineAnimalsCytotoxic T cellImmunology and AllergyCell LineageMOLIMMUNOOligonucleotide Array Sequence AnalysisB-LymphocytesT follicular helper cell differentiationbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingInterleukinsInterleukin-17ProteinsGerminal centerCell DifferentiationT-Lymphocytes Helper-InducerTransforming growth factor betaFlow CytometryGerminal CenterAdoptive TransferImmunohistochemistryMolecular biologyMice Mutant Strainsmedicine.anatomical_structureInfectious DiseasesT helper 1CELLIMMUNOImmunologybiology.proteinInterleukin 17Signal TransductionImmunity
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Shikonin promotes intestinal wound healing in vitro via induction of TGF-β release in IEC-18 cells

2013

The intestinal barrier is a complex system with a dynamic structure that is designed for the maintenance of homeostasis in healthy individuals. Ulcerative colitis, one of the main manifestations of inflammatory bowel disease, is characterized by an inadequate and delayed wound healing. Shikonin, the active principle in the root of Lithospermum erythrorhizon, has demonstrated its ability to attenuate dextran sulfate sodium-induced ulcerative colitis in mice. Moreover, the root of L. erythrorhizon has been used in traditional Chinese medicine for treatment of burns, anal ulcers, hemorrhoids and skin wounds. However, the effect of shikonin on intestinal wound healing is unknown. Using an in vi…

STAT3 Transcription FactorCell SurvivalPharmaceutical SciencePharmacologyInflammatory bowel diseaseCell Linechemistry.chemical_compoundCell MovementTransforming Growth Factor betamedicineAnimalsSTAT3Wound HealingCrohn's diseaseintegumentary systembiologybusiness.industryAnti-Inflammatory Agents Non-SteroidalTranscription Factor RelACell migrationNF-κBLithospermum erythrorhizonbiology.organism_classificationmedicine.diseaseUlcerative colitisRatsIntestineschemistryImmunologybiology.proteinWound healingbusinessNaphthoquinonesEuropean Journal of Pharmaceutical Sciences
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