Search results for "Peroxisome Proliferator-Activated Receptor"

showing 10 items of 123 documents

Astrocytes Protect Neurons from Aβ1-42 Peptide-Induced Neurotoxicity Increasing TFAM and PGC-1 and Decreasing PPAR-γ and SIRT-1

2015

One of the earliest neuropathological events in Alzheimer's disease is accumulation of astrocytes at sites of Aβ1-42 depositions. Our results indicate that Aβ1-42 toxic peptide increases lipid peroxidation, apoptosis and cell death in neurons but not in astrocytes in primary culture. Aβ1-42-induced deleterious neuronal effects are not present when neurons and astrocytes are mixed cultured. Stimulation of astrocytes with toxic Aβ1-42 peptide increased p-65 and decreased IκB resulting in inflammatory process. In astrocytes Aβ1-42 decreases protein expressions of sirtuin 1 (SIRT-1) and peroxisome proliferator-activated receptor γ (PPAR-γ) and over-expresses peroxisome proliferator-activated re…

MnSODProgrammed cell deathPPAR-γPeroxisome proliferator-activated receptorMitochondrionBiologyBioinformaticsmedicine.disease_causeAlzheimer's DiseaseNeurologiaPGC-1Sirtuin 1medicineAnimalsTFAMCells Culturedchemistry.chemical_classificationNeuronsAmyloid beta-PeptidesCell DeathSirtuin 1Caspase 3Superoxide DismutaseNeurotoxicityTranscription Factor RelAGeneral MedicineTFAMmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCoculture TechniquesPeptide FragmentsCell biologyMitochondriaPeroxidesRatsPPAR gammachemistryMitochondrial biogenesisNF-κB.Astrocytesbiology.proteinFisiologia humanaLipid PeroxidationOxidative stressResearch PaperTranscription FactorsInternational Journal of Medical Sciences
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PPAR-γ Agonist GW1929 But Not Antagonist GW9662 Reduces TBBPA-Induced Neurotoxicity in Primary Neocortical Cells

2013

Tetrabromobisphenol A (2,2-bis(4-hydroxy-3,5-dibromophenyl)propane; TBBPA) is a widely used brominated flame retardant. TBBPA induces neuronal damage, but the mechanism by which this occurs is largely unknown. We studied the possible involvement of peroxisome proliferator-activated receptor gamma (PPAR-γ) in TBBPA-induced apoptosis and toxicity in mouse primary neuronal cell cultures. TBBPA enhanced both, caspase-3 activity and lactate dehydrogenase (LDH) release in neocortical cells after 6 and 24 h of exposition. These data were supported at the cellular level with Hoechst 33342 staining. Immunoblot analyses showed that, compared with control cells, 10 μM TBBPA decreased the expression of…

PPAR-γTime FactorsNeuroscience(all)Polybrominated BiphenylsPeroxisome proliferator-activated receptorGW1929Caspase 3ApoptosisNeocortexPharmacologyBiologyToxicologyNeuroprotectionBenzophenonesMicemedicineNeurotoxicityAnimalsAnilidesReceptorCells Culturedchemistry.chemical_classificationNeuronsDose-Response Relationship DrugL-Lactate DehydrogenaseCaspase 3General NeuroscienceNeurotoxicityApoptotic bodymedicine.diseasePPAR gammaTBBPANeuroprotective AgentschemistryCell cultureApoptosisTyrosineNeurotoxicity SyndromesOriginal ArticleCentral Nervous System AgentsNeurotoxicity Research
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Myoglobin, expressed in brown adipose tissue of mice, regulates the content and activity of mitochondria and lipid droplets

2021

Abstract The identification of novel physiological regulators that stimulate energy expenditure through brown adipose tissue (BAT) activity in substrate catalysis is of utmost importance to understand and treat metabolic diseases. Myoglobin (MB), known to store or transport oxygen in heart and skeletal muscles, has recently been found to bind fatty acids with physiological constants in its oxygenated form (i.e., MBO2). Here, we investigated the in vivo effect of MB expression on BAT activity. In particular, we studied mitochondrial function and lipid metabolism as essential determinants of energy expenditure in this tissue. We show in a MB-null (MBko) mouse model that MB expression in BAT i…

PalmitatesOxidative phosphorylationMitochondrion1307 Cell BiologyMiceAdipose Tissue BrownLipid dropletBrown adipose tissueRespiration1312 Molecular BiologymedicineAnimalsHumansPPAR alpha11434 Center for Clinical StudiesMuscle SkeletalMolecular BiologyUncoupling Protein 1Mice KnockoutMyoglobinChemistryProteinsThermogenesisLipid metabolismLipid DropletsCell BiologyMetabolism10081 Institute of Veterinary PhysiologyPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaCell biologyOxygenDisease Models AnimalAdipocytes Brownmedicine.anatomical_structure10076 Center for Integrative Human Physiology570 Life sciences; biologyApoptosis Regulatory ProteinsEnergy MetabolismThermogenesisBiochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
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The Blood–Brain Barrier as a Target in Traumatic Brain Injury Treatment

2014

Traumatic brain injury (TBI) is one of the most frequent causes of death in the young population. Several clinical trials have unsuccessfully focused on direct neuroprotective therapies. Recently immunotherapeutic strategies shifted into focus of translational research in acute CNS diseases. Cross-talk between activated microglia and blood–brain barrier (BBB) could initiate opening of the BBB and subsequent recruitment of systemic immune cells and mediators into the brain. Stabilization of the BBB after TBI could be a promising strategy to limit neuronal inflammation, secondary brain damage and acute neurodegeneration. This review provides an overview on the pathophysiology of TBI and brain…

Pathologymedicine.medical_specialtyTraumatic brain injuryPeroxisome Proliferator-Activated ReceptorsBrain EdemaInflammationBrain damageBlood–brain barrierNeuroprotectionRosiglitazoneReceptors GlucocorticoidmedicineHumansHypoglycemic AgentsMyosin-Light-Chain KinaseNeuroinflammationInflammationPioglitazoneMicrogliabusiness.industryNeurodegenerationNeurodegenerative DiseasesGeneral Medicinemedicine.diseaseCell HypoxiaNeuroprotective Agentsmedicine.anatomical_structurenervous systemBlood-Brain BarrierBrain InjuriesThiazolidinedionesmedicine.symptombusinessNeuroscienceArchives of Medical Research
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The human peroxisome in health and disease: The story of an oddity becoming a vital organelle

2013

Abstract Since the first report by Rhodin in 1954, our knowledge on mammalian microbodies/peroxisomes has known several periods. An initial two decades period (1954–1973) has contributed to the biochemical individualisation of peroxisomes as a new class of subcellular organelles (de Duve, 1965). The corresponding research period failed to define a clear role of mammalian peroxisomes in vital functions and intermediary metabolism, explaining why feeling that peroxisomes might be in the human cell oddities has prevailed during several decades. The period standing from 1973 to nowadays has progressively removed this cell oddity view of peroxisomes by highlighting vital function and metabolic r…

Peroxisome Proliferator-Activated ReceptorsDiseaseBiologyCell FractionationMicrobodiesBiochemistryPeroxisomal DisordersOrganellePeroxisomal disorderCentrifugation Density GradientPeroxisomesmedicineAnimalsHumansMicrobodyZellweger SyndromeOrganelle envelopeFatty AcidsGeneral MedicinePeroxisomeLipid Metabolismmedicine.diseaseCell biologyBiochemistryNuclear receptorMetabolic Networks and PathwaysFunction (biology)Biochimie
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Natural products and analogs as preventive agents for metabolic syndrome via peroxisome proliferator-activated receptors: An overview.

2021

Abstract Natural products and synthetic analogs have drawn much attention as potential therapeutical drugs to treat metabolic syndrome. We reviewed the underlying mechanisms of 32 natural products and analogs with potential pharmacological effects in vitro, and especially in rodent models and/or patients, that usually act on the PPAR pathway, along with other molecular targets. Recent outstanding total syntheses or semisyntheses of these lead compounds are stated. In general, they can activate the transcriptional activity of PPARα, PPARγ, PPARα/γ, PPARβ/δ, PPARα/δ, PPARγ/δ and panPPAR as weak, partial agonists or selective PPARγ modulators (SPPARγM), which may be useful for managing obesity…

Peroxisome Proliferator-Activated ReceptorsPeroxisome proliferator-activated receptorPharmacologyResveratrol01 natural sciences03 medical and health scienceschemistry.chemical_compoundStructure-Activity RelationshipBerberineDrug DiscoverymedicineAnimalsHumansReceptor030304 developmental biologyPharmacologychemistry.chemical_classificationMetabolic Syndrome0303 health sciencesBiological ProductsDose-Response Relationship DrugMolecular Structure010405 organic chemistryChemistryOrganic ChemistryGeneral MedicinePPAR Pathwaymedicine.disease0104 chemical sciencesCurcuminQuercetinDyslipidemiaEuropean journal of medicinal chemistry
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Phosphorylation of peroxisome proliferator-activated receptor α in rat Fao cells and stimulation by ciprofibrate

1999

The basic mechanism(s) by which peroxisome proliferators activate peroxisome proliferator-activated receptors (PPARs) is (are) not yet fully understood. Given the diversity of peroxisome proliferators, several hypotheses of activation have been proposed. Among them is the notion that peroxisome proliferators could activate PPARs by changing their phosphorylation status. In fact, it is well known that several members of the nuclear hormone receptor superfamily are regulated by phosphorylation. In this report, we show that the rat Fao hepatic-derived cell line, known to respond to peroxisome proliferators, exhibited a high content of PPARalpha. Alkaline phosphatase treatment of Fao cell lysat…

Peroxisome proliferator-activated receptor gammaPhosphataseReceptors Cytoplasmic and NuclearPeroxisome proliferator-activated receptorBiologyMicrobodiesBiochemistryCell LineClofibric AcidmedicineAnimalsEnzyme InhibitorsPhosphorylationPharmacologychemistry.chemical_classificationFibric Acidsfood and beveragesPeroxisomePhosphoric Monoester HydrolasesRatsGene Expression RegulationBiochemistryNuclear receptorchemistryPhosphorylationPeroxisome Proliferatorslipids (amino acids peptides and proteins)Acyl-CoA OxidasePeroxisome proliferator-activated receptor alphaCiprofibrateOxidoreductasesTranscription Factorsmedicine.drugBiochemical Pharmacology
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The analysis of modified peroxisome proliferator responsive elements of the peroxisomal bifunctional enzyme in transfected HepG2 cells reveals two re…

1995

AbstractPeroxisome proliferators (PPs) are non-genotoxic carcinogens in rodents. They can induce the expression of numerous genes via the heterodimerization of two members of the steroid hormone receptor superfamily, called the peroxisome proliferator-activated receptor (PPAR) and the 9-cis retinoic acid receptor (RXR). Many of the PP responsive genes possess a peroxisome proliferator response element (PPRE) formed by two TGACCT-related motifs. The bifunctional enzyme (HD) PPRE contains 3 such motifs, creating DR1 and DR2 sequences. PPAR and RXR regulate transcription via the DR1 element while DR2 modulates the expression of the gene via auxiliary factors in HepG2 cells.

Peroxisome proliferator-activated receptor gammaReceptors Retinoic AcidSteroid hormone receptorMolecular Sequence DataResponse elementBiophysicsReceptors Cytoplasmic and NuclearPeroxisome proliferator-activated receptorchemical and pharmacologic phenomenaIn Vitro TechniquesRegulatory Sequences Nucleic AcidRetinoid X receptorBiologyPeroxisomal Bifunctional EnzymeTransfectionMicrobodiesBiochemistryGene Expression Regulation EnzymologicTranscriptional activationPeroxisomal Bifunctional EnzymeMultienzyme ComplexesStructural BiologyPeroxisome proliferator response element9-cis Retinoic acid receptor alphaTumor Cells CulturedGeneticsHumansRNA MessengerIsomerasesEnoyl-CoA HydrataseMolecular Biologychemistry.chemical_classificationBinding SitesBase Sequence3-Hydroxyacyl CoA DehydrogenasesPeroxisome proliferator-activated receptorCell BiologyDNA-Binding ProteinsRetinoic acid receptorRetinoid X ReceptorsLiverOligodeoxyribonucleotidesBiochemistrychemistryRat peroxisomal enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenaseEnzyme InductionPeroxisome proliferator-activated receptor alphaTranscription FactorsFEBS Letters
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Functional characterization of a peroxisome proliferator response-element located in the intron 3 of rat peroxisomal thiolase B gene.

2003

Expression of the rat peroxisomal 3-ketoacyl-CoA thiolase gene B is induced by peroxisome proliferators. Although a sequence element like a peroxisome proliferator-activated receptor (PPAR)-binding site is located in the promoter region of this gene, we previously found that this element is competent for the activation by hepatocyte nuclear factor-4, but not functional with PPARalpha. We describe here a new peroxisome proliferator-response element located in the intron 3 (+1422/+1434) that binds in vitro the PPARalpha/retinoid X receptor alpha heterodimer and confers the induction by PPARalpha in transfection assays. We propose a model of regulation of the rat thiolase B gene involving thos…

Peroxisome proliferator-activated receptor gammaResponse elementBiophysicsPeroxisome proliferator-activated receptorReceptors Cytoplasmic and NuclearRetinoid X receptorBiochemistryGene Expression Regulation EnzymologicStructure-Activity RelationshipPeroxisomesAnimalsAcetyl-CoA C-AcetyltransferaseMolecular BiologyCells Culturedchemistry.chemical_classificationThiolaseChemistryCell BiologyPhosphoproteinsMolecular biologyIntronsRatsDNA-Binding ProteinsBiochemistryHepatocyte Nuclear Factor 4LiverPeroxisome proliferator-activated receptor deltaPeroxisome ProliferatorsPeroxisome proliferator-activated receptor alphaPPARGC1BTranscription FactorsBiochemical and biophysical research communications
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Argan oil prevents down-regulation induced by endotoxin on liver fatty acid oxidation and gluconeogenesis and on peroxisome proliferator-activated re…

2015

In patients with sepsis, liver metabolism and its capacity to provide other organs with energetic substrates are impaired. This and many other pathophysiological changes seen in human patients are reproduced in mice injected with purified endotoxin (lipopolysaccharide, LPS). In the present study, down-regulation of genes involved in hepatic fatty acid oxidation (FAOx) and gluconeogenesis in mice exposed to LPS was challenged by nutritional intervention with Argan oil. Mice given a standard chow supplemented or not with either 6% (w/w) Argan oil (AO) or 6% (w/w) olive oil (OO) prior to exposure to LPS were explored for liver gene expressions assessed by mRNA transcript levels and/or enzyme a…

Peroxisome proliferator-activated receptor gammamedicine.medical_specialtyOO olive oilResearch paper[SDV]Life Sciences [q-bio]Peroxisome proliferator-activated receptorBiologyBiochemistryNuclear receptor 30lcsh:BiochemistryEstrogen-related receptorEstrogen-related receptor alphaInternal medicineACADS acyl CoA dehydrogenase short-chainACADL acyl CoA dehydrogenase long-chainmedicinePGC-1α peroxisome proliferator-activated receptor γ coactivator-1αlcsh:QD415-436ReceptorBeta oxidationHNF-4α hepatic nuclear factor-4αchemistry.chemical_classificationACADM acyl CoA dehydrogenase medium-chainPPARα peroxisome proliferator-activated receptor αERRα estrogen related receptor α[ SDV ] Life Sciences [q-bio]PEPCK phospoenolpyruvate carboxykinaseGluconeogenesisBeta-oxidationGlut4 glucose transporter 4[SDV] Life Sciences [q-bio]G6PH glucose-6-phosphataseEndocrinologyGlut2 glucose transporter 2chemistryNuclear receptorArgan oilAO Argan oilNuclear receptorACOX1 acyl-CoA oxidase 1CoactivatorLPS lipopolysaccharidePeroxisome proliferator-activated receptor alpha
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