Search results for " A2"

showing 10 items of 160 documents

Membrane breakdown in acute and chronic neurodegeneration: focus on choline-containing phospholipids.

2000

Breakdown of cellular membranes is a characteristic feature of neuronal degeneration in acute (stroke) and chronic (senile dementia) neurological disorders. The present review summarizes recent experimental and clinical work which concentrated on changes of choline-containing phospholipids as indicators of neuronal membrane breakdown. Experimental studies identified glutamate release, calcium influx, and activation of cellular phospholipase A2 (PLA2) as important steps initiating membrane breakdown in cultured neurons or brain slices under hypoxic or ischemic conditions. Proton NMR studies have shown an elevation of choline-containing compounds in the brain of Alzheimer patients while neuro…

PhospholipidPhospholipasechemistry.chemical_compoundNeurochemicalPhospholipase A2PhosphatidylcholinemedicineCholineAnimalsHumansBiological PsychiatrybiologyChemistryNeurodegenerationCell MembraneGlutamate receptorNeurodegenerative Diseasesmedicine.diseasePsychiatry and Mental healthNeurologyBiochemistryAcute DiseaseChronic Diseasebiology.proteinPhosphatidylcholinesNeurology (clinical)Journal of neural transmission (Vienna, Austria : 1996)
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Plasmalogens in the retina: From occurrence in retinal cell membranes to potential involvement in pathophysiology of retinal diseases

2014

Plasmalogens (Pls) represent a specific subclass of glycerophospholipids characterized by the presence of a vinyl-ether bond at the sn-1 position of glycerol. Pls are quantitatively important in membranes of neuronal tissues, including the brain and the retina, where they can represent until almost two-third of ethanolamine glycerophospholipids. They are considered as reservoirs of polyunsaturated fatty acids as several studies have shown that arachidonic and docosahexaenoic acids are preferentially esterified on Pls when compared to other glycerophospholipids. Reduced levels of Pls were observed in a number of neurodegenerative disorders such as glaucoma, the second leading cause of blindn…

PlasmalogensGlycerophospholipidsBiochemistryMicrophthalmiaRetinachemistry.chemical_compoundPhospholipase A2Retinal DiseasesPhospholipase A2[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicineAnimalsHumans[SDV.MHEP.OS]Life Sciences [q-bio]/Human health and pathology/Sensory OrgansPhospholipidschemistry.chemical_classificationRetinabiologyCell MembraneGlaucomaOptic NerveRetinalGeneral Medicinemedicine.diseaseeye diseasesBiosynthetic Pathways3. Good healthmedicine.anatomical_structureBiochemistrychemistryDocosahexaenoic acid[ SDV.MHEP.OS ] Life Sciences [q-bio]/Human health and pathology/Sensory OrgansOptic nervebiology.proteinPolyunsaturated fatty acidsAngiogenesissense organs[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyPolyunsaturated fatty acidBiochimie
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Development of a second generation of inhibitors of microsomal prostaglandin E synthase 1 expression bearing the γ-hydroxybutenolide scaffold

2008

Petrosaspongiolide M (PM), a marine sesterterpene metabolite bearing the gamma-hydroxybutenolide scaffold and displaying a potent inhibitory activity toward PLA(2) enzyme, was selected by us as an attractive target in order to explore its mechanism of action at molecular level. In the course of our investigations we decided to synthetically modify the parent compound to clarify the structural determinants responsible for the activity; in fact, very recently, our research group reported the synthesis and the pharmacological properties of a first collection of PM analogues generated by Ludi approach. The synthesized compounds showed a poor or moderate activity toward PLA(2) enzymes, neverthel…

Prostaglandin AntagonistsStereochemistryMetaboliteClinical BiochemistryAnti-Inflammatory AgentsPharmaceutical ScienceIsomeraseProstaglandin E synthaseBiochemistryChemical synthesisCell LineMiceStructure-Activity Relationshipchemistry.chemical_compound4-ButyrolactoneMicrosomesDrug DiscoverymedicineAnimalsEnzyme InhibitorsProstaglandin E2Molecular BiologyProstaglandin-E Synthaseschemistry.chemical_classificationBinding SitesbiologyChemistryMacrophagesOrganic ChemistryIntramolecular OxidoreductasesPhospholipases A2EnzymeGene Expression RegulationMechanism of actionBiochemistryCyclooxygenase 2Enzyme inhibitorbiology.proteinMolecular Medicinelipids (amino acids peptides and proteins)medicine.symptommedicine.drugBioorganic & Medicinal Chemistry
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PLA2-mediated catalytic activation of its inhibitor 25-acetyl-petrosaspongiolide M: serendipitous identification of a new PLA2 suicide inhibitor.

2004

Abstract25-Acetyl-petrosaspongiolide M (PMAc) (1), a mild non-covalent PLA2 inhibitor, unexpectedly recovers, after incubation with bvPLA2, the ability to covalently modify the enzyme target. This study demonstrates the catalytic effect of bvPLA2 in converting 1 in its deacetylated congener petrosaspongiolide M (PM) (2), a strong covalent PLA2 inhibitor whose molecular mechanism of inhibition has already been clarified. Moreover, our findings outline the potential role of PMAc as anti-inflammatory pro-drug, by virtue of its ability of delivering the active PM agent at the site of inflammation, functioning as a suicide inhibitor.

Protein ConformationMarine natural productLigandsBiochemistryMass SpectrometryProtein Structure SecondaryCIRCULAR-DICHROISMchemistry.chemical_compoundProtein structureStructural BiologyBINDINGEnzyme InhibitorsChromatography High Pressure Liquidchemistry.chemical_classificationbiologyMolecular StructureChemistryCircular DichroismHydrolysisTemperatureAcetylationHydrogen-Ion ConcentrationBEE VENOM PHOSPHOLIPASE-A2PoriferaPETROSASPONGIOLIDES M-RBiochemistryCovalent bondINACTIVATIONMANOALIDESpectrometry Mass Electrospray IonizationCYTOSOLIC PHOSPHOLIPASE A(2); BEE VENOM PHOSPHOLIPASE-A2; FLUORESCENCE DISPLACEMENT ASSAY; PETROSASPONGIOLIDES M-R; CIRCULAR-DICHROISM; NATURAL-PRODUCTS; INACTIVATION; MANOALIDE; POTENT; BINDINGStereochemistryBiophysicsGroup II Phospholipases A2CatalysisPhospholipases AAnti-inflammatory compoundManoalidePhospholipase A2NATURAL-PRODUCTSGeneticsTrifluoroacetic acidAnimalsBinding siteOleanolic AcidMolecular BiologyBinding SitesPOTENTCYTOSOLIC PHOSPHOLIPASE A(2)Cell BiologyMolecular WeightKineticsPhospholipases A2EnzymeAcetylationbiology.proteinFLUORESCENCE DISPLACEMENT ASSAYPhospholipase A2 inhibitionFEBS letters
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Sialotranscriptomics of the argasid tick ornithodoros moubata along the trophogonic cycle

2021

32 páginas, 8 tablas, 6 figuras

Proteomics0301 basic medicineSwinePhysiologyRC955-962Gene ExpressionDisease VectorsProteomicsBiochemistryTranscriptomeMedical Conditions0302 clinical medicineTicksArctic medicine. Tropical medicineGene expressionMedicine and Health SciencesHuman relapsing feverGeneticsbiologyEukaryotaGenomicsProteasesBody FluidsEnzymesBloodInfectious DiseasesFemaleMetabolic PathwaysAnatomyPublic aspects of medicineRA1-1270Transcriptome analysisVitellogeninsMetabolic Networks and PathwaysResearch ArticleIxodidaeArthropoda030231 tropical medicineTickSalivary glandsArthropod Proteins03 medical and health sciencesExocrine GlandsOrnithodoros moubataArachnidaGeneticsAnimalsXenobiotic MetabolismTick ControlOrnithodorosSalivaIllumina dye sequencingIxodesAsfarviridaeImmunityOrganismsPublic Health Environmental and Occupational HealthBiology and Life SciencesComputational BiologyProteinsGenome Analysisbiology.organism_classificationInvertebratesOrnithodoros moubataPhospholipases A2Species InteractionsMetabolism030104 developmental biologyAfricaEnzymologyMetalloproteasesAfrican swine feverTranscriptomeDigestive SystemZoology
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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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Therapeutic modulation of lipoprotein-associated phospholipase A2 (Lp-PLA2)

2011

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a calcium-independent phospholipase A2 that circulates in plasma in association with lipoprotein particles, whereas in atherosclerotic plaques it is co-localized with macrophages. Lp-PLA2 generates two proinflammatory mediators, lysophosphatidylcholine and oxidized nonesterified fatty acids, which play a role in the development of atherosclerotic lesions and formation of a necrotic core, leading to more vulnerable plaques. Epidemiologic studies demonstrate that increased circulating levels of Lp-PLA2 predict an increased risk of myocardial infarction, stroke and cardiovascular mortality. Furthermore, histologic examination of diseased hum…

RiskPathologymedicine.medical_specialtycoronary-artery-diseasecardiovascular-diseasePharmacologyatherosclerotic plaqueProinflammatory cytokinechemistry.chemical_compoundPhospholipase A2cardiovascular diseaseDarapladibOximesDrug DiscoveryHyperlipidemiamedicineHumansMyocardial infarctionPharmacologyClinical Trials as Topicbiologylow-density-lipoproteinLipoprotein-associated phospholipase A2risk-assessmentCardiovascular AgentsAtherosclerosismedicine.diseaselp-pla2heart-diseaselipoproteinsLysophosphatidylcholinechemistryCardiovascular DiseasesinflammationBenzaldehydes1-Alkyl-2-acetylglycerophosphocholine Esterasebiology.proteindarapladibrheumatoid-arthritislipids (amino acids peptides and proteins)atherosclerosisfactor-acetylhydrolase activityAtherosclerosis Cardiovascular disease Darapladib Inflammation Lipoproteins Lp-PLA2.platelet-activating-factorsecondary preventionLipoprotein
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Gathering of aging and estrogen withdrawal in vascular dysfunction of senescent accelerated mice.

2010

The aim of this work was to characterize a mouse model of experimental menopause and cardiovascular aging that closely reflects menopause in women. Senescence accelerated mouse (SAM)-Resistant type 1 (SAMR1, n=30) and SAM-Prone type 8 (SAMP8, n=30) were separated at 5months of age into three groups: 1) sham-operated (Sham); 2) ovariectomized (Ovx); and 3) ovariectomized chronically-treated with estrogen (Ovx+E2). Contractile responses to KCl (60mM) and thromboxane A(2) were greater in aorta from SAMP8 mice compared with SAMR1 in all groups. Neither ovariectomy nor estrogen replacement modified the contractile responses from SAMR1 mice. Conversely, in Ovx SAMP8 the increased maximal contract…

SenescenceAgingmedicine.medical_specialtyEndotheliummedicine.drug_classThromboxaneOvariectomyVasodilator AgentsDown-RegulationIn Vitro TechniquesNitric OxideBiochemistryReceptors Thromboxane A2 Prostaglandin H2Thromboxane A2chemistry.chemical_compoundMiceEndocrinologyInternal medicineGeneticsmedicineAnimalsVasoconstrictor AgentsEnzyme InhibitorsMolecular BiologyAortaEstradiolChemistryEstrogen Replacement TherapyAging PrematureEstrogensCell Biologymedicine.diseaseAcetylcholineMenopauseVasodilationEndocrinologymedicine.anatomical_structureNG-Nitroarginine Methyl EsterEstrogenVasoconstriction15-Hydroxy-11 alpha9 alpha-(epoxymethano)prosta-513-dienoic AcidOvariectomized ratBlood VesselsFemalehormones hormone substitutes and hormone antagonistsAcetylcholinemedicine.drugExperimental gerontology
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Lipoprotein-associated phospholipase A2 activity is increased in patients with definite familial hypercholesterolemia compared with other forms of hy…

2018

Background and Aim: Lipoprotein-associated phospholipase A2(Lp-PLA2) plays a key role in atherosclerosis development. It is considered a marker of increased risk of cardiovascular disease (CVD) and plaque vulnerability. Familial hypercholesterolemia (FH) is a genetic disorder characterized by elevated plasma levels of low-density lipoprotein cholesterol and a higher prevalence of early CVD. Our aim was to evaluate the differences in Lp-PLA2activity in a population of hypercholesterolemic patients with and without definite FH. Methods and Results: Hypercholesterolemic patients were consecutively recruited. Definite FH was defined according to Dutch Lipid Clinic Network criteria ≥8. All pat…

Settore MED/09 - Medicina InternaStatin treatmentEndocrinology Diabetes and MetabolismFamilial hypercholesterolemiaNutrition and DieteticMedicine (miscellaneous)Low density lipoproteinCardiovascular diseaseCardiovascular riskLipoprotein-associated phospholipase A2Plaque vulnerabilityCardiology and Cardiovascular MedicineVascular inflammation
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Selective killing of human monocytes and cytokine release provoked by sphingomyelinase (beta-toxin) of Staphylococcus aureus.

1996

The best-known activity of Staphylococcus aureus sphingomyelinase C, alias beta-toxin, is as a hemolysin that provokes hot-cold lysis of erythrocytes which contain substantial amounts of sphingomyelin in the plasma membrane. Sheep erythrocytes are most susceptible, and we found that one hemolytic unit, representing the toxin concentration that elicits 50% hemolysis of 2.5 X 10(8) erythrocytes per ml, corresponds to 0.05 enzyme units or to approximately 0.25 microg of sphingomyelinase per ml. The cytotoxic action of beta-toxin on nucleated cells has not been described in any detail before, and the present investigation was undertaken to fill this information gap. We now identify beta-toxin a…

Staphylococcus aureusTime FactorsLipopolysaccharideCD14ImmunologyBacterial ToxinsLipopolysaccharide ReceptorsExotoxinsMicrobiologyMonocytesMicrobiologychemistry.chemical_compoundHemolysin ProteinsPhospholipase A2Antigens CDmedicineHumansbiologyCell DeathDose-Response Relationship DrugCytotoxinsMonocyteHemolysinReceptors Interleukinmedicine.diseaseReceptors Interleukin-6HemolysisInfectious Diseasesmedicine.anatomical_structureSphingomyelin PhosphodiesteraseMechanism of actionchemistrybiology.proteinCytokinesParasitologymedicine.symptomSphingomyelinResearch ArticleInterleukin-1
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