Search results for "Retinoid"

showing 10 items of 79 documents

Vitamin E activates CRABP-II gene expression in cultured human fibroblasts, role of protein kinase C

2004

The treatment of human fibroblasts with different tocopherols in the presence of retinol caused an increase in cytoplasmic retinoic acid binding protein II (CRABP-II) mRNA and protein. The possibility of an involvement of protein kinase C (PKC) in the response to tocopherols was supported by the results obtained with the PKC-specific inhibitors, calphostin C and bisindolylmaleimide I. The effect of alpha-tocopherol was prevented by okadaic acid, suggesting that a protein phosphatase is responsible for PKC dephosphorylation produced by the presence of tocopherols. The results shown support the hypothesis that phosphorylation/dephosphorylation of RXRalpha via PKC may be involved in the regula…

MaleBisindolylmaleimideTranscription GeneticReceptors Retinoic AcidPhosphatasealpha-TocopherolBiophysicsBiochemistryDephosphorylationchemistry.chemical_compoundStructural BiologyProtein kinase COkadaic AcidGeneticsHumansVitamin ERNA MessengerRetinoic acid bindingPhosphorylationMolecular BiologyProtein kinase CCells CulturedDNA PrimersBase SequenceReverse Transcriptase Polymerase Chain ReactionInfant NewbornRetinoid X receptor αCell BiologyMolecular biologyRetinoic acid receptorCalphostin CchemistryGene Expression RegulationProtein phosphatasePhosphorylationFibroblastCytoplasmic retinoic acid binding protein IIFEBS Letters
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ApoB100,LDLR-/- mice exhibit reduced electroretinographic response and cholesteryl esters deposits in the retina

2008

International audience; PURPOSE. To evaluate the retinal phenotype of 7- and 14-month-old apoB100,LDLR–/– mice, a relevant animal model of lipid metabolism dysfunction. METHODS. Single-flash electroretinograms were obtained from 7- and 14-month-old apoB100,LDLR–/– and control mice fed a standard diet under both scotopic and photopic conditions. Visual cycle retinoids were analyzed in eyes from dark-adapted mice. Retinal and choroidal vascularization was evaluated with scanning laser ophthalmoscopy. Fatty acids were analyzed in the retina. Esterified and free cholesterol was detected in eye cryosections. RESULTS. Scotopic and photopic b-wave amplitudes were significantly reduced in apoB100,L…

MaleHUMAN BRUCHS MEMBRANEgenetic structuresHIGH-FAT DIETLipid Metabolism DisordersBasement MembraneAGE-RELATED MACULOPATHYchemistry.chemical_compoundMice0302 clinical medicine[SDV.IDA]Life Sciences [q-bio]/Food engineeringFluorescein AngiographyPigment Epithelium of EyeTRANSGENIC MICE0303 health sciencesmedicine.diagnostic_testROD OUTER SEGMENTSmedicine.anatomical_structureBiochemistryHUMAN APOLIPOPROTEIN-BApolipoprotein B-100Femalelipids (amino acids peptides and proteins)Cholesterol EstersPhotopic visionVisual phototransductionmedicine.medical_specialtyDark AdaptationMice TransgenicBiologyRetinaRECEPTOR-NEGATIVE MICE03 medical and health sciencesRetinoidsRetinal DiseasesBASAL DEPOSITSInternal medicinemedicineElectroretinographyAnimals[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringFilipinHUMAN ATHEROSCLEROTIC LESIONS030304 developmental biologyRetinaRetinal pigment epitheliumRetinalMacular degenerationmedicine.diseaseMACULAR DEGENERATIONeye diseasesMice Inbred C57BLOphthalmoscopyEndocrinologychemistryReceptors LDLLDL receptor030221 ophthalmology & optometrysense organsPhotic StimulationElectroretinography
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Induction of the fatty acid transport protein 1 and acyl-CoA synthase genes by dimer-selective rexinoids suggests that the peroxisome proliferator-ac…

2000

The intracellular fatty acid content of insulin-sensitive target tissues determines in part their insulin sensitivity. Uptake of fatty acids into cells is a controlled process determined in part by a regulated import/export system that is controlled at least by two key groups of proteins, i.e. the fatty acid transport protein (FATP) and acyl-CoA synthetase (ACS), which facilitate, respectively, the transport of fatty acids across the cell membrane and catalyze their esterification to prevent their efflux. Previously it was shown that the expression of the FATP-1 and ACS genes was controlled by insulin and by peroxisome proliferator-activated receptor (PPAR) agonists in liver or in adipose t…

MalePeroxisome proliferator-activated receptor gammaTime FactorsReceptors Retinoic AcidRetinoic acidReceptors Cytoplasmic and NuclearPeroxisome proliferator-activated receptorTretinoinRetinoid X receptorBiologyFatty Acid-Binding ProteinsBiochemistryMicechemistry.chemical_compoundCoenzyme A LigasesTumor Cells CulturedAnimalsHumansTissue DistributionMolecular BiologyNucleic Acid Synthesis InhibitorsCell Nucleuschemistry.chemical_classificationDose-Response Relationship DrugFatty AcidsMembrane ProteinsFatty acidMembrane Transport ProteinsSerum Albumin Bovine3T3 CellsCell BiologyFatty Acid Transport ProteinsRatsRats ZuckerRetinoic acid receptorRetinoid X ReceptorschemistryBiochemistryDactinomycinFree fatty acid receptorRNAPeroxisome proliferator-activated receptor alphaCaco-2 CellsCarrier ProteinsTranscription Factors
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Toxicological Profile of Ultrapure 2,2´,3,4,4´,5,5´-Heptachlorbiphenyl (PCB 180) in Adult Rats

2014

PCB 180 is a persistent non-dioxin-like polychlorinated biphenyl (NDL-PCB) abundantly present in food and the environment. Risk characterization of NDL-PCBs is confounded by the presence of highly potent dioxin-like impurities. We used ultrapure PCB 180 to characterize its toxicity profile in a 28-day repeat dose toxicity study in young adult rats extended to cover endocrine and behavioral effects. Using a loading dose/maintenance dose regimen, groups of 5 males and 5 females were given total doses of 0, 3, 10, 30, 100, 300, 1000 or 1700 mg PCB 180/kg body weight by gavage. Dose-responses were analyzed using benchmark dose modeling based on dose and adipose tissue PCB concentrations. Body w…

MalePhysiologyAdipose tissueTHYROID-HORMONEPOSTNATAL EXPOSURE010501 environmental sciences413 Veterinary scienceToxicologyPathology and Laboratory Medicine01 natural sciencesBiochemistryRats Sprague-DawleyFollicle-stimulating hormoneHemoglobinsMedicine and Health SciencesEFFECT-DIRECTED ANALYSIS0303 health scienceseducation.field_of_studyMultidisciplinaryBehavior AnimalMaintenance doseQRNeurochemistryAnemiaNeurotransmittersHematologyPolychlorinated BiphenylsToxicokineticsAdipose TissueHematocritLiverToxicityBlood ChemistryMedicineEnvironmental PollutantsFemaleLuteinizing hormoneResearch ArticleARYL-HYDROCARBON RECEPTORNeurotoxicologymedicine.medical_specialtyThyroid HormonesPOLYCHLORINATED-BIPHENYLS PCBSScienceeducationPopulationToxic Agentsta3111Loading dose03 medical and health sciencesRetinoidsSex FactorsInternal medicinemedicineSex HormonesDEVELOPMENTAL EXPOSUREAnimalseducationToxic equivalency factorMolecular Biology030304 developmental biology0105 earth and related environmental sciencesToxicityDose-Response Relationship DrugDIBENZO-P-DIOXINSBody WeightBiology and Life SciencesIN-VITROKemiLuteinizing HormoneHormonesRatsDIOXIN-LIKE-PCBSEndocrinologyChemical SciencesAdrenal CortexExploratory BehaviorSUBCHRONIC TOXICITYFollicle Stimulating HormoneDNA Damage
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Activation of the Constitutive Androstane Receptor Inhibits Leukocyte Adhesiveness to Dysfunctional Endothelium

2021

Leukocyte cell recruitment into the vascular subendothelium constitutes an early event in the atherogenic process. As the effect of the constitutive androstane receptor (CAR) on leukocyte recruitment and endothelial dysfunction is poorly understood, this study investigated whether the role of CAR activation can affect this response and the underlying mechanisms involved. Under physiological flow conditions, TNFα-induced endothelial adhesion of human leukocyte cells was concentration-dependently inhibited by preincubation of human umbilical arterial endothelial cells with the selective human CAR ligand CITCO. CAR agonism also prevented TNFα induced VCAM-1 expression, as well as MCP-1/CCL-2 a…

MaleSmall interfering RNAEndotheliumQH301-705.5Receptors Cytoplasmic and NuclearVascular Cell Adhesion Molecule-1Leukocyte RollingRetinoid X receptorArticleendothelial dysfunctionCatalysisInorganic ChemistryMiceConstitutive androstane receptorCell AdhesionHuman Umbilical Vein Endothelial CellsLeukocytesmedicineAnimalsHumansBiology (General)Physical and Theoretical ChemistryEndothelial dysfunctionQD1-999Molecular BiologySpectroscopyconstitutive androstane receptorTumor Necrosis Factor-alphaChemistryOrganic ChemistryNF-kappa BEndothelial Cellsleukocyte recruitmentGeneral Medicinemedicine.diseaseComputer Science ApplicationsCell biologyChemistrymedicine.anatomical_structureGene Expression RegulationTumor necrosis factor alphaIntravital microscopySignal TransductionInternational Journal of Molecular Sciences
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Thyroid hormone induction of the adrenoleukodystrophy-related gene (ABCD2).

2003

X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VLCFA) beta-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3'-tri-iodothyronine (T3) receptor (TRbeta) as a heterodimer and mediating T3 responsiveness of ABCD2 in its promoter conte…

MaleThyroid HormonesReceptors Retinoic AcidGene ExpressionATP-binding cassette transporterRetinoid X receptorRats Sprague-DawleyMiceABCD3Gene expressionABCD2medicineAnimalsHumansReceptorAdrenoleukodystrophyPromoter Regions GeneticGeneCells CulturedRepetitive Sequences Nucleic AcidPharmacologyChemokine CCL22Mice KnockoutReceptors Thyroid Hormonebiologymedicine.diseaseCell biologyRatsUp-RegulationOligodendrogliaRetinoid X ReceptorsLiverAstrocytesChemokines CCbiology.proteinCancer researchMolecular MedicineTriiodothyronineAdrenoleukodystrophyChemokine CCL17Transcription FactorsMolecular pharmacology
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The murine nuclear orphan receptor GCNF is expressed in the XY body of primary spermatocytes

1998

AbstractWe have studied the expression of the nuclear orphan receptor GCNF (germ cell nuclear factor) on the mRNA and protein level in pubertal and adult mouse testes. We show by Northern and Western blot analyses and by in situ hybridization that GCNF is expressed in spermatocytes and round spermatids of adult mouse testis suggesting that GCNF may be a transcriptional regulator of spermatogenesis. Since the GCNF protein is accumulated in the XY body of late pachytene spermatocytes, it may be involved in transcriptional inactivation of sex chromosomes.

MaleTranscription GeneticGerm cell nuclear factorBiophysicsFluorescent Antibody TechniqueReceptors Cytoplasmic and NuclearIn situ hybridizationBiologyIn Vitro TechniquesGerm cell nuclear factorBiochemistryEpitheliumMiceWestern blotStructural BiologySpermatocytesNuclear Receptor Subfamily 6 Group A Member 1TestisGeneticsTranscriptional regulationmedicineAnimalsRNA MessengerRetinoid receptor-related testis-associated receptorSpermatogenesisMolecular BiologyOrphan receptorMessenger RNAMice Inbred BALB Cmedicine.diagnostic_testCell BiologyMolecular biologySpermatidsNeuron-derived orphan receptor 1DNA-Binding ProteinsGene Expression RegulationNuclear orphan receptorSpermatogenesisNeuronal cell nuclear factorXY bodyFEBS Letters
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Vitamin D Receptor Activation Reduces Angiotensin-II–Induced Dissecting Abdominal Aortic Aneurysm in Apolipoprotein E–Knockout Mice

2015

Objective— Abdominal aortic aneurysm (AAA) is a vascular disorder characterized by chronic inflammation of the aortic wall. Low concentrations of vitamin D 3 are associated with AAA development; however, the potential direct effect of vitamin D 3 on AAA remains unknown. This study evaluates the effect of oral treatment with the vitamin D 3 receptor (VDR) ligand, calcitriol, on dissecting AAA induced by angiotensin-II (Ang-II) infusion in apoE −/− mice. Approach and Results— Oral treatment with calcitriol reduced Ang-II–induced dissecting AAA formation in apoE −/− mice, which was unrelated to systolic blood pressure or plasma cholesterol concentrations. Immunohistochemistry and reverse-tran…

MaleVascular Endothelial Growth Factor A0301 basic medicineDissecting Abdominal Aortic Aneurysm030204 cardiovascular system & hematologyLigandsCalcitriol receptorchemistry.chemical_compound0302 clinical medicineAorta AbdominalCells CulturedMice KnockoutAngiotensin IIVascular endothelial growth factorChemotaxis LeukocyteVascular endothelial growth factor APhenotypeMatrix Metalloproteinase 9Vitamin D3 ReceptorMatrix Metalloproteinase 2RNA Interferencelipids (amino acids peptides and proteins)ChemokinesMitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineSignal Transductionmedicine.drugmedicine.medical_specialtyCalcitriolBiologyTransfectionProinflammatory cytokine03 medical and health sciencesApolipoproteins ECalcitriolInternal medicineHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansGenetic Predisposition to DiseaseRetinoid X Receptor alphaMacrophagesAngiotensin IIMice Inbred C57BLAortic DissectionDisease Models Animal030104 developmental biologyEndocrinologychemistryReceptors CalcitriolAortic Aneurysm AbdominalArteriosclerosis, Thrombosis, and Vascular Biology
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Vitamin A Deficiency Increases Protein Catabolism and Induces Urea Cycle Enzymes in Rats

2010

Chronic vitamin A deficiency induces a substantial delay in the rates of weight and height gain in both humans and experimental animals. This effect has been associated with an impaired nutrient metabolism and loss of body protein. Therefore, we analyzed the effect of vitamin A deficiency on endogenous proteolysis and nitrogen metabolism and its reversibility with all-trans retinoic acid (RA). Male weanling rats, housed in pairs, were pair-fed a vitamin A-deficient (VAD) or control diet until they were 60 d old. A group of deficient rats were further treated with daily intraperitoneal injections of all-trans RA for 10 d. Final body and tissue (i.e. liver and heart) weights were significantl…

MaleVitaminmedicine.medical_specialtyNitrogenMedicine (miscellaneous)TretinoinBiologyAntioxidantsRetinoidschemistry.chemical_compoundInternal medicinemedicineAnimalsUreaMuscle SkeletalTriglyceridesNutrition and DieteticsVitamin A DeficiencyCatabolismRetinolProtein turnoverMethylhistidinesmedicine.diseaseRatsVitamin A deficiencyProtein catabolismEndocrinologyLiverchemistryEnzyme InductionUrea cycleLipid PeroxidationEnergy sourceThe Journal of Nutrition
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Retinol, at concentrations greater than the physiological limit, induces oxidative stress and apoptosis in human dermal fibroblasts

2004

We have investigated the dose (in the range of microM) and time-dependent effects of four different retinoids (retinol, retinal, retinoic acid and retinol palmitate) on human dermal fibroblasts cultivated in vitro. Retinol and retinal, at a concentration of 20 microM, caused cell damage as evaluated by lactate dehydrogenase activity released into the culture medium. The oxidised glutathione (GSSG)/reduced glutathione (GSH) ratio and malondialdehyde production indicated that 20 microM of retinol provoked oxidative stress in the cultivated human fibroblasts. In the first 8 h after retinol treatment the levels of p53 and Bax proteins as well as caspase 3 activity increased, suggesting apoptoti…

Malemedicine.medical_specialtyAntioxidantmedicine.medical_treatmentRetinoic acidApoptosisTretinoinDermatologyBiologymedicine.disease_causeBiochemistryAntioxidantsRetinoidschemistry.chemical_compoundSkin Physiological PhenomenaInternal medicinemedicineHumansVitamin AMolecular BiologyCells CulturedSkinCell DeathDose-Response Relationship DrugGlutathione DisulfideL-Lactate DehydrogenaseVitamin EInfant NewbornRetinolRetinalGlutathioneFibroblastsMalondialdehydeGlutathioneOxidative StressEndocrinologychemistryOxidative stressExperimental Dermatology
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