Search results for "IPT"

showing 10 items of 6114 documents

CD16+ Macrophages Mediate Fibrosis in Inflammatory Bowel Disease.

2017

Background and Aims Fibrosis is a common complication of Crohn's disease [CD], and is related to dysregulated tissular repair following inflammation, in which macrophages play a central role. We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. In the present study, we analyse the role of STAT6-dependent macrophages in intestinal fibrosis. Methods Colitis was induced by weekly intra-rectal administration of TNBS [6 weeks] to STAT6-/- mice and wild-typ…

0301 basic medicineMaleCell CountInflammatory bowel diseaseMiceCrohn DiseaseFibrosisMacrophageIntestinal MucosaCells CulturedMice Knockouteducation.field_of_studyMice Inbred BALB Cintegumentary systemGastroenterologyGeneral MedicineColitisColonic NeoplasmsFemalemedicine.symptomMannose ReceptorAdultAdolescentColonPopulationInflammationReceptors Cell SurfaceCD1603 medical and health sciencesYoung AdultProto-Oncogene Proteinsparasitic diseasesmedicineAnimalsHumansLectins C-TypeColitiseducationInterleukin 4business.industryMacrophagesReceptors IgGmedicine.diseaseFibrosisWnt Proteins030104 developmental biologyMannose-Binding LectinsTrinitrobenzenesulfonic AcidImmunologyInterleukin-4businessSTAT6 Transcription FactorJournal of Crohn'scolitis
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The maternal hormone in the male brain: Sexually dimorphic distribution of prolactin signalling in the mouse brain.

2018

Research of the central actions of prolactin is highly focused on females, but this hormone has also documented roles in male physiology and behaviour. Here, we provide the first description of the pattern of prolactin-derived signalling in the male mouse brain, employing the immunostaining of phosphorylated signal transducer and activator of transcription 5 (pSTAT5) after exogenous prolactin administration. Next, we explore possible sexually dimorphic differences by comparing pSTAT5 immunoreactivity in prolactin-supplemented males and females. We also assess the role of testosterone in the regulation of central prolactin signalling in males by comparing intact with castrated prolactin-supp…

0301 basic medicineMaleCell signalingPeptide HormonesSignal transductionBiochemistrychemistry.chemical_compoundMice0302 clinical medicineArcuate NucleusSTAT5 Transcription FactorMedicine and Health SciencesMorphogenesisTestosteroneLipid HormonesPhosphorylationTestosteroneNeuronsSex CharacteristicsMultidisciplinarySexual DifferentiationCerebrumReproductionQRBrainHormones esteroidesSTAT signalingmedicine.anatomical_structureCervell Localització de funcionsHypothalamusAndrogensMedicineFemaleAnatomyhormones hormone substitutes and hormone antagonistsResearch Articlemedicine.medical_specialtyendocrine systemCell biologyScienceHypothalamusBiologyResearch and Analysis MethodsAmygdala03 medical and health sciencesInternal medicinemedicineAnimalsCastrationImmunohistochemistry TechniquesSexual DimorphismProlactin receptorBiology and Life SciencesProlactinHormonesProlactinSexual dimorphismHistochemistry and Cytochemistry Techniques030104 developmental biologyEndocrinologyCastrationchemistryImmunologic Techniques030217 neurology & neurosurgeryHormoneDevelopmental BiologyPloS one
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LXR agonist treatment of blastic plasmacytoid dendritic cell neoplasm restores cholesterol efflux and triggers apoptosis

2016

International audience; Blastic plasmacytoid dendritic cell (PDC) neoplasm (BPDCN) is an aggressive hematological malignancy with a poor prognosis that derives from PDCs. No consensus for optimal treatment modalities is available today and the full characterization of this leukemia is still emerging. We identified here a BPDCN-specific transcriptomic profile when compared with those of acute myeloid leukemia and T-acute lymphoblastic leukemia, as well as the transcriptomic signature of primary PDCs. This BPDCN gene signature identified a dysregulation of genes involved in cholesterol homeostasis, some of them being liver X receptor (LXR) target genes. LXR agonist treatment of primary BPDCN …

0301 basic medicineMaleCellProliferationApoptosisExpressionPlasmacytoid dendritic cellPrecursor T-Cell Lymphoblastic Leukemia-LymphomaBiochemistryMice0302 clinical medicinepolycyclic compoundsSTAT5 Transcription Factor[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyATP Binding Cassette Transporter Subfamily G Member 1Liver X ReceptorsInhibitionMyeloid NeoplasiabiologyMyeloid leukemiafood and beveragesMyeloid-Leukemia[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematologyInterleukin-3 Receptor3. Good healthLeukemiamedicine.anatomical_structureCholesterol030220 oncology & carcinogenesisFemalelipids (amino acids peptides and proteins)In-VivoATP Binding Cassette Transporter 1ImmunologyActivationAntineoplastic Agentsdigestive system03 medical and health sciencesCell Line TumormedicineAnimalsHumansLiver X receptorProtein kinase BCell ProliferationCell growthCell BiologyDendritic Cellsmedicine.diseaseXenograft Model Antitumor Assays030104 developmental biologyProstate-Cancer CellsABCA1biology.proteinCancer researchDensity-Lipoprotein ReceptorInterleukin-3Proto-Oncogene Proteins c-akt
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Cohesin-dependent regulation of gene expression during differentiation is lost in cohesin-mutated myeloid malignancies.

2019

Cohesin complex disruption alters gene expression, and cohesin mutations are common in myeloid neoplasia, suggesting a critical role in hematopoiesis. Here, we explore cohesin dynamics and regulation of hematopoietic stem cell homeostasis and differentiation. Cohesin binding increases at active regulatory elements only during erythroid differentiation. Prior binding of the repressive Ets transcription factor Etv6 predicts cohesin binding at these elements and Etv6 interacts with cohesin at chromatin. Depletion of cohesin severely impairs erythroid differentiation, particularly at Etv6-prebound loci, but augments self-renewal programs. Together with corroborative findings in acute myeloid le…

0301 basic medicineMaleCohesin complexChromosomal Proteins Non-HistoneImmunologyGene DosageCell Cycle ProteinsBiologyRegulatory Sequences Nucleic AcidBiochemistryHistones03 medical and health sciences0302 clinical medicineNeoplasmshemic and lymphatic diseasesCell Line TumorBiomarkers TumorHumansTranscription factorRegulation of gene expressionHematopoietic stem cell homeostasisMyeloid NeoplasiaMyeloproliferative DisordersCohesinProto-Oncogene Proteins c-etsGene Expression Regulation LeukemicETS transcription factor familyMyeloid leukemiafood and beveragesCell BiologyHematologyHematopoietic Stem CellsCell biologyChromatinHematopoiesisRepressor Proteins030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisMutationFemalesense organsbiological phenomena cell phenomena and immunityNeoplasm GradingBLOOD CommentaryProtein BindingBlood
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Novel multiple sclerosis susceptibility loci implicated in epigenetic regulation

2016

Genome-wide study in Germans identifies four novel multiple sclerosis risk genes and confirms already known gene loci.

0301 basic medicineMaleDLEU1MedizinGenome-wide association studyEpigenesis GeneticCohort StudiesResearch ArticlesTranscriptional Regulator ERGGeneticsAged 80 and overGlycine Hydroxymethyltransferaseeducation.field_of_studyMultidisciplinaryDNA methylationSciAdv r-articlesMiddle AgedSHMT13. Good healthddc:DNA-Binding ProteinsERGDNA methylationFemaleMAZFunction and Dysfunction of the Nervous SystemResearch ArticleAdultAdolescentPopulationQuantitative Trait Loci610 Medicine & healthDleu1 ; Dna Methylation ; Erg ; L3mbtl3 ; Maz ; Multiple Sclerosis ; Shmt1 ; Genome-wide Association StudyQuantitative trait locusBiologyMajor histocompatibility complexNeurological DisordersMultiple sclerosis03 medical and health sciencesYoung AdultTranscriptional Regulator ERGHumansGenetic Predisposition to DiseaseL3MBTL3EpigeneticsAlleleeducationAllelesAgedgenome-wide association study030104 developmental biologyGenetic LociCase-Control Studiesbiology.proteinTranscription Factors
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Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin.

2020

Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in mammalian brain. In clinical settings, recombinant EPO treatment has revealed a remarkable improvement of cognition, but underlying mechanisms have remained obscure. Here, we show with a novel line of reporter mice that cognitive challenge induces local/endogenous hypoxia in hippocampal pyramidal neurons, hence enhancing expression of EPO and EPO receptor (EPOR). High-dose EPO administration, amplifying auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single-cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, i…

0301 basic medicineMaleDendritic spineGeneral Physics and AstronomyHippocampal formationVARIANTSADULT NEUROGENESIS0302 clinical medicineCognitionhemic and lymphatic diseasesReceptors ErythropoietinHypoxialcsh:ScienceNEURONSMultidisciplinaryNeuronal PlasticityPyramidal CellsNeurogenesisQBrainCell DifferentiationHEMATOPOIETIC PROGENITOR CELLSFemalemedicine.symptomProto-Oncogene Proteins c-fosmedicine.drugEXPRESSIONScienceDendritic SpinesNeurogenesisModels NeurologicalBiologyMotor ActivityGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesParacrine signallingPhysical Conditioning AnimalNeuroplasticitymedicineAnimalsHumansErythropoietinMEMORYCognitive neuroscienceGeneral ChemistryHypoxia (medical)RECOMBINANT-HUMAN-ERYTHROPOIETINCellular neuroscienceErythropoietin receptorMice Inbred C57BLMICE030104 developmental biologyErythropoietinPhysical EnduranceIDENTITYlcsh:QTranscriptomeNeuroscience030217 neurology & neurosurgeryGene Deletion
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Urinary- and Plasma-Derived Exosomes Reveal a Distinct MicroRNA Signature Associated With Albuminuria in Hypertension.

2021

Urinary albumin excretion (UAE) is a marker of cardiovascular risk and renal damage in hypertension. MicroRNAs (miRNAs) packaged into exosomes function as paracrine effectors in cell communication and the kidney is not exempt. This study aimed to state an exosomal miRNA profile/signature associated to hypertension with increased UAE and the impact of profibrotic TGF-β1 (transforming growth factor β1) on exosomes miRNA release. Therefore, exosomes samples from patients with hypertension with/without UAE were isolated and characterized. Three individual and unique small RNA libraries from each subject were prepared (total plasma, urinary, and plasma-derived exosomes) for next-generation sequ…

0301 basic medicineMaleDown-Regulation030204 cardiovascular system & hematologyExosomesTransforming Growth Factor beta103 medical and health sciencesParacrine signalling0302 clinical medicinemicroRNAInternal MedicinemedicineAlbuminuriaHumansGene Regulatory NetworksKEGGCells CulturedAgedKidneybusiness.industryPodocytesReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingMiddle AgedMicrovesiclesMicroRNAs030104 developmental biologyReal-time polymerase chain reactionmedicine.anatomical_structureHypertensionAlbuminuriaCancer researchFemalemedicine.symptombusinessTransforming growth factorHypertension (Dallas, Tex. : 1979)
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Blimp1 Prevents Methylation of Foxp3 and Loss of Regulatory T Cell Identity at Sites of Inflammation

2018

Summary Foxp3+ regulatory T (Treg) cells restrict immune pathology in inflamed tissues; however, an inflammatory environment presents a threat to Treg cell identity and function. Here, we establish a transcriptional signature of central nervous system (CNS) Treg cells that accumulate during experimental autoimmune encephalitis (EAE) and identify a pathway that maintains Treg cell function and identity during severe inflammation. This pathway is dependent on the transcriptional regulator Blimp1, which prevents downregulation of Foxp3 expression and “toxic” gain-of-function of Treg cells in the inflamed CNS. Blimp1 negatively regulates IL-6- and STAT3-dependent Dnmt3a expression and function …

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalBlimp1CNS2Regulatory T cellInflammationchemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyArticleepigenetic regulationDNA Methyltransferase 3AEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineImmune systemDownregulation and upregulationmedicineAnimalsEpigeneticsDNA (Cytosine-5-)-Methyltransferaseslcsh:QH301-705.5Regulation of gene expressionInterleukin-6FOXP3Forkhead Transcription FactorsDNA methyltransferaseshemic and immune systemsDNA Methylation3. Good healthCell biologyddc:Mice Inbred C57BL030104 developmental biologymedicine.anatomical_structureregulatory T cellslcsh:Biology (General)inflammationFoxp3DNA methylationFemalePositive Regulatory Domain I-Binding Factor 1medicine.symptomCNS030217 neurology & neurosurgeryCell Reports
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Expression quantitative trait loci for PAX8 contributes to the prognosis of hepatocellular carcinoma

2017

Paired-box family member PAX8 encodes a transcription factor that has a role in cell differentiation and cell growth and may participate in the prognosis of hepatocellular carcinoma (HCC). By bioinformatics analysis, we identified several single nucleotide polymorphisms (SNPs) within a newly identified long non-coding RNA (lncRNA) AC016683.6 as expression quantitative trait loci (eQTLs) for PAX8. Hence, we hypothesized that PAX8eQTLs in lncRNA AC016683.6 may influence the HCC prognosis. We then performed a case-only study to assess the association between the two SNPs as well as the prognosis of HCC in 331 HBV-positive HCC patients without surgical treatment. Cox proportional hazard models …

0301 basic medicineMaleHeredityPaired BoxCancer Treatmentlcsh:MedicineBiochemistry0302 clinical medicineMathematical and Statistical TechniquesMedicine and Health Scienceslcsh:ScienceMultidisciplinaryPharmaceuticsLiver DiseasesLiver NeoplasmsMiddle AgedPrognosisNucleic acidsSurvival RateGenetic MappingOncology030220 oncology & carcinogenesisHepatocellular carcinomaPhysical SciencesRegression AnalysisFemaleLiver cancerStatistics (Mathematics)Research ArticleCarcinoma HepatocellularGenotypeQuantitative Trait LociSingle-nucleotide polymorphismVariant GenotypesGastroenterology and HepatologyResearch and Analysis MethodsCarcinomasPolymorphism Single Nucleotide03 medical and health sciencesPAX8 Transcription FactorProtein DomainsDrug TherapyDiagnostic MedicineGastrointestinal TumorsCarcinomamedicineGeneticsChemotherapyHumansGenetic Predisposition to DiseaseAlleleStatistical MethodsNon-coding RNASurvival rateSurvival analysisAllelesbusiness.industrylcsh:RCancers and NeoplasmsBiology and Life SciencesProteinsHepatocellular Carcinomamedicine.disease030104 developmental biologyExpression quantitative trait lociCancer researchLong non-coding RNAsRNAlcsh:QbusinessMathematicsPLoS ONE
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Generation of a disease-specific iPS cell line derived from a patient with Charcot-Marie-Tooth type 2K lacking functional GDAP1 gene

2016

Human CMT2-FiPS4F1 cell line was generated from fibroblasts of a patient with Charcot-Marie-Tooth disease harbouring the following mutations in the GDAP1 gene in heterozygosis: p.Q163X/p.T288NfsX3. This patient did not present mutations in the PM22, MPZ or GJB genes. Human reprogramming factors OCT3/4, KLF4, SOX2 and C-MYC were delivered using a non-integrative methodology that involves the use of Sendai virus.

0301 basic medicineMaleHeterozygoteCellular differentiationCèl·lulesDNA Mutational AnalysisGenetic VectorsInduced Pluripotent Stem CellsKaryotypeNerve Tissue ProteinsBiologyPolymorphism Single NucleotideSendai virusCell Line03 medical and health sciencesKruppel-Like Factor 4stomatognathic systemCharcot-Marie-Tooth DiseaseHumansInduced pluripotent stem cellGeneTranscription factorMedicine(all)GeneticsBase SequenceHeterozygote advantageCell DifferentiationCell BiologyGeneral MedicineFibroblastsbiology.organism_classificationCellular ReprogrammingSendai virus030104 developmental biologyMicroscopy FluorescenceKLF4embryonic structuresSistema nerviós MalaltiesReprogrammingDevelopmental BiologyTranscription Factors
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