Search results for "fibroblast"

showing 10 items of 667 documents

Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Hormones of Energy Balance in a TCDD-Sensitive and a TCDD-Resistant Rat Strain

2014

One of the hallmarks of the acute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a drastically reduced feed intake by an unknown mechanism. To further elucidate this wasting syndrome, we followed the effects of a single large dose (100 μg/kg) of TCDD on the serum levels of several energy balance-influencing hormones, clinical chemistry variables, and hepatic aryl hydrocarbon receptor (AHR) expression in two rat strains that differ widely in their TCDD sensitivities, for up to 10 days. TCDD affected most of the analytes in sensitive Long-Evans rats, while there were few alterations in the resistant Han/Wistar strain. However, analyses of feed-restricted unexposed Long-Evans rats i…

LeptinFOOD-INTAKETCDDFGF21Polychlorinated Dibenzodioxinsmedicine.medical_treatmentAHRwasting syndromeacute toxicity413 Veterinary science8-tetrachlorodibenzo-p-dioxinlcsh:Chemistry2378-tetrachlorodibenzo-<i>p</i>-dioxin; TCDD; wasting syndrome; energy balance; hormones; acute toxicity; strain differences; AHRPPAR-ALPHAInsulinMESSENGER-RNA EXPRESSIONInsulin-Like Growth Factor Ita315Receptorlcsh:QH301-705.5AH RECEPTORSpectroscopyenergiatasebiologyChemistryLeptinGeneral MedicineCENTRAL LEPTIN INFUSIONstrain differencesComputer Science ApplicationsLiverGhrelinAdiponectinARYL-HYDROCARBON RECEPTOR7medicine.medical_specialty3education2GlucagonCatalysisArticleInorganic ChemistrySpecies SpecificityInternal medicinemedicineAnimals2378-tetrachlorodibenzo-p-dioxinRats Long-EvansRNA MessengerPhysical and Theoretical ChemistryRats WistarCARBOXYKINASE PEPCK ACTIVITYMolecular BiologyI IGF-IhormonesGrowth factorOrganic ChemistryBody WeightAryl hydrocarbon receptorGlucagonenergy balancehormonitRatsFibroblast Growth FactorsEndocrinologylcsh:Biology (General)lcsh:QD1-999Receptors Aryl Hydrocarbonbiology.proteinGROWTH-FACTOR 21Energy MetabolismHormoneInternational Journal of Molecular Sciences
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Modulation of protein tyrosine nitration and inflammatory mediators by isoprenylhydroquinone glucoside.

2007

The nitration of tyrosine caused by peroxynitrite and other reactive nitrogen species is clearly detrimental for some physiological processes; however, its signalling role is still open to controversy. Among the natural phenolics known for their ability to oppose free tyrosine nitration, isoprenylhydroquinone glucoside is investigated due to its unusual structure, which contains a simple hydroxybenzene alkylated by a hemiterpenoid moiety. This hydroquinone was shown to be an effective inhibitor of peroxynitrite-induced protein tyrosine nitration in 3T3 fibroblasts. When tested on bovine seroalbumin nitration, however, the potency was reduced by half and the effect was almost abolished in th…

LipopolysaccharidesCell SurvivalNeutrophilsBlotting WesternInterleukin-1betaPharmaceutical ScienceNitric Oxide Synthase Type IIHemeNitric oxidechemistry.chemical_compoundMiceGlucosideGlucosidesNitrationPeroxynitrous AcidAnimalsHumansTyrosineReactive nitrogen speciesCells CulturedNitritesNitratesbiologyCell-Free SystemReverse Transcriptase Polymerase Chain ReactionRhodaminesTumor Necrosis Factor-alphaNitrotyrosineSerum Albumin Bovine3T3 CellsHydrogen PeroxideFibroblastsStimulation ChemicalHydroquinonesNitric oxide synthasechemistryBiochemistrybiology.proteinTetradecanoylphorbol AcetateTyrosineInflammation MediatorsPeroxynitriteEuropean journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
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FACIT collagen (1α-chain) is expressed by hemocytes and epidermis during the inflammatory response of the ascidian Ciona intestinalis

2007

Based on previous cloning and sequencing study, real-time PCR and in situ hybridization assays of the inflamed body wall of LPS-injected Ciona intestinalis showed the enhanced gene expression of a collagen with FACIT structural features (Ci-type IX-Col 1alpha-chain). By using specific antibodies raised against an opportunely chosen Ci-type IX-Col synthetic peptide, the fibroblast property of hemocytes challenged in vitro with LPS (at 4h) was displayed by flow cytometry, while immunocytochemistry identified hemocytes with large granules (morula cells) as collagen-producing cells. Hemocyte lysate supernatant analyzed in immunoblotting contained a 60 kDa band identifiable as 1alpha-chain-Ci-ty…

LipopolysaccharidesHemocytesImmunologyImmunocytochemistryIn situ hybridizationCollagen Type IXFACIT collagenExtracellular matrixParacrine CommunicationEscherichia colimedicineAnimalsCiona intestinalisFibroblastIn Situ HybridizationInflammationbiologyEpidermis (botany)Gene Expression Profilingbiology.organism_classificationImmunohistochemistryMolecular biologyCiona intestinalisExtracellular Matrixmedicine.anatomical_structureEpidermal CellsImmunologyEpidermisWound healingProtein Processing Post-TranslationalProcollagenDevelopmental BiologyDevelopmental &amp; Comparative Immunology
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Interaction of dicaffeoylquinic derivatives with peroxynitrite and other reactive nitrogen species.

2008

Plant phenolic antioxidants, among them catechins and hydroxycinnamoyl conjugates, constitute a well defined class of inhibitors of reactive nitrogen species (RNS). To gain deeper insight in this field, we examined the effects of 3,5-di-O-caffeoylquinic acid (DCA), its methyl ester (DCE) and epigallocatechin gallate (EGCG) in nitrative and oxidative processes. These compounds were found to be strong inhibitors of the nitration of tyrosine residues induced by ONOO- in bovine seroalbumin, with their IC50 values (10-40 microM) notably decreasing in the presence of bicarbonate. When studied on the intracellular protein tyrosine nitration induced by ONOO- in cultured murine fibroblasts as well a…

LipopolysaccharidesNeutrophilsBicarbonateBiophysicsQuinic AcidNitric Oxide Synthase Type IIEpigallocatechin gallateBiochemistryCatechinNitric oxidechemistry.chemical_compoundInhibitory Concentration 50MiceNitrationPeroxynitrous AcidAnimalsHumansTyrosineMolecular BiologyReactive nitrogen speciesNitritesNitratesNitrotyrosineMacrophagesSerum Albumin BovineFibroblastsReactive Nitrogen SpeciesStimulation ChemicalBicarbonateschemistryBiochemistryTetradecanoylphorbol AcetateTyrosineCattleOxidation-ReductionPeroxynitriteArchives of biochemistry and biophysics
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Evolving therapies for liver fibrosis

2013

Fibrosis is an intrinsic response to chronic injury, maintaining organ integrity when extensive necrosis or apoptosis occurs. With protracted damage, fibrosis can progress toward excessive scarring and organ failure, as in liver cirrhosis. To date, antifibrotic treatment of fibrosis represents an unconquered area for drug development, with enormous potential but also high risks. Preclinical research has yielded numerous targets for antifibrotic agents, some of which have entered early-phase clinical studies, but progress has been hampered due to the relative lack of sensitive and specific biomarkers to measure fibrosis progression or reversal. Here we focus on antifibrotic approaches for li…

Liver CirrhosisPathologymedicine.medical_specialtyCirrhosisT-LymphocytesInflammationApoptosisBioinformaticsMonocytesMiceFibrosismedicineHepatic Stellate CellsAnimalsHumansMyofibroblastsInflammationWound Healingbusiness.industryLiver DiseasesMacrophagesStem CellsReview SeriesGeneral Medicinemedicine.diseaseFibrosisClinical trialDrug developmentLiverHepatic stellate cellDisease ProgressionHepatocytesStem cellmedicine.symptombusinessWound healingBiomarkers
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Targeted therapy of liver fibrosis/cirrhosis and its complications.

2011

Department of Pharmacokinetics, Toxicology, and Targeting, University of Groningen, Antonius Deusinglaan 1, 9713 AV, Groningen, The Netherlands; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA; Division of Molecular and Translational Medicine, Johannes Gutenberg University, Langenbeckstr. 1, 55131 Mainz, Germany

Liver Cirrhosismedicine.medical_specialtyCirrhosisMacrophageKupffer CellsLiver fibrosismedicine.medical_treatmentKupffer cellTargeted therapyMyoblastsDrug Delivery SystemsInternal medicinemedicineHepatic Stellate CellsHumansHepatocyteMolecular Targeted TherapyHCCMyofibroblastTargetingDrug CarriersHepatologybusiness.industryGeneral surgeryAntifibrotic therapyMedical schoolTranslational medicineHepatologyFibroblastsmedicine.diseaseFibrosisLiverStellate cellHepatocytesDrugbusinessCholangiocyteJournal of hepatology
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Liver fibrosis induced by hepatic overexpression of PDGF-B in transgenic mice

2006

Background/Aims In hepatic fibrogenesis, stellate cells are activated leading to production and deposition of extracellular matrix. To clarify the role of PDGF-B in liver fibrogenesis, we overexpressed PDGF-B in the liver of transgenic mice. Methods Transgenic mice for the conditional overexpression of PDGF-B in the liver under control of an albumin promoter were generated utilising the Cre/loxP system. Constitutive PDGF-B expression was achieved after breeding with mice expressing Cre-recombinase under actin promoter control. Tamoxifen inducible expression was achieved after breeding with mice expressing Cre under transthyretin receptor promoter control. Levels of fibrosis were assessed an…

Liver Cirrhosismedicine.medical_specialtyPlatelet-derived growth factorLiver cytologyTransgeneMice TransgenicBiologyMicechemistry.chemical_compoundTransforming Growth Factor betaFibrosisInternal medicinemedicineAnimalsPromoter Regions GeneticCells CulturedCell ProliferationIntegrasesHepatologyTransdifferentiationCell DifferentiationProto-Oncogene Proteins c-sisFibroblastsmedicine.diseaseExtracellular MatrixEndocrinologyGene Expression RegulationLiverchemistryHepatocytesCancer researchHepatic stellate cellHepatic fibrosisMyofibroblastJournal of Hepatology
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Fibroblast Growth Factor 21 Limits Lipotoxicity by Promoting Hepatic Fatty Acid Activation in Mice on Methionine and Choline-Deficient Diets

2014

Background & Aims Nonalcoholic fatty liver disease is a common consequence of human and rodent obesity. Disruptions in lipid metabolism lead to accumulation of triglycerides and fatty acids, which can promote inflammation and fibrosis and lead to nonalcoholic steatohepatitis. Circulating levels of fibroblast growth factor (FGF)21 increase in patients with nonalcoholic fatty liver disease or nonalcoholic steatohepatitis; therefore, we assessed the role of FGF21 in the progression of murine fatty liver disease, independent of obesity, caused by methionine and choline deficiency. Methods C57BL/6 wild-type and FGF21-knockout (FGF21-KO) mice were placed on methionine- and choline-deficient (MCD)…

Liver Cirrhosismedicine.medical_specialtyTime FactorsBiologyInfusions SubcutaneousSeverity of Illness IndexArticleHepatitischemistry.chemical_compoundAcyl-CoAMethionineNon-alcoholic Fatty Liver DiseaseInternal medicineNonalcoholic fatty liver diseasemedicineAnimalsRNA MessengerMice Knockoutchemistry.chemical_classificationHepatologyFatty acid metabolismFatty AcidsFatty liverGastroenterologyFatty acidmedicine.diseaseRecombinant ProteinsCholine DeficiencyFibroblast Growth FactorsMice Inbred C57BLDisease Models AnimalEndocrinologyLiverchemistryLipotoxicityDisease ProgressionLipid PeroxidationInflammation MediatorsSteatosisLong chain fatty acidOxidation-ReductionGastroenterology
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NR1H4 rs35724 G>C variant modulates liver damage in nonalcoholic fatty liver disease

2021

Background and Aims: Farnesoid X receptor (FXR) plays a key role in bile acid and lipid homeostasis. Experimental evidence suggests that it can modulate liver damage related to nonalcoholic fatty liver disease (NAFLD). We examined the impact of the NR1H4 rs35724 G&gt;C, encoding for FXR, on liver damage in a large cohort of patients at risk of steatohepatitis. Methods: We considered 2,660 consecutive individuals at risk of steatohepatitis with liver histology. The rs35724 G&gt;C polymorphisms were genotyped by TaqMan assays. Gene expression was evaluated by RNASeq in a subset of patients (n = 124). Results: The NR1H4 rs35724 CC genotype, after adjusting for clinic-metabolic and genetic conf…

Liver Cirrhosismedicine.medical_specialtymedicine.drug_classReceptors Cytoplasmic and NuclearGastroenterologyBile Acids and Saltschemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseFibrosisSettore BIO/13 - Biologia ApplicataInternal medicineNAFLDNonalcoholic fatty liver diseasemedicineHumansReceptor Fibroblast Growth Factor Type 4Settore MED/12 - GastroenterologiaHepatologyBile acidCholesterolbusiness.industryNASHObeticholic acidmedicine.diseaseNR1H4LiverchemistryFXRSteroid HydroxylasesFarnesoid X receptorSteatohepatitisSteatosisbusiness
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DPP-4 is overexpressed in lung tissue from idiopathic pulmonary patients and activates lung fibroblasts

2020

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible form of fibrotic interstitial lung disease, characterized by uncontrolled fibroblast invasion. Dipeptidyl peptidase-4 (DPP-4)/ glucagon-like peptide 1 (GLP-1) system is involved in multiple effects, including cardiac, liver or kidney fibrosis. However, its implication in IPF has not been described. Objective: To analyse the implication of DPP4/GLP1 system in IPF. Methods: Protein expression of DPP4, GLP-1 and GLP-1 receptor was analyzed in lung tissues from 7 IPF patients. TGFβ1-induced fibroblast to myofibroblast transition (FMT), epithelial to mesenchymal transition (EMT) and mesothelial to mesenchymal trans…

Lungbusiness.industrydigestive oral and skin physiologyInterstitial lung diseaserespiratory systemmedicine.diseaserespiratory tract diseasesCTGFIdiopathic pulmonary fibrosismedicine.anatomical_structureSitagliptinCancer researchmedicineEpithelial–mesenchymal transitionbusinessMyofibroblastDipeptidyl peptidase-4medicine.drugIdiopathic interstitial pneumonias
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