Search results for "lysophosphatidylcholine"

showing 10 items of 20 documents

Expressional control of the ‘constitutive’ isoforms of nitric oxide synthase (NOS I and NOS III)

1998

Nitric oxide synthase (NOS) exists in three established isoforms. NOS I (NOS1, ncNOS) was originally discovered in neurons. This enzyme and splice variants thereof have since been found in many other cells and tissues. NOS II (NOS2, iNOS) was first identified in murine macrophages, but can also be induced in many other cell types. NOS III (NOS3, ecNOS) is expressed mainly in endothelial cells. Whereas NOS II is a transcriptionally regulated enzyme, NOS I and NOS III are considered constitutively expressed proteins. However, evidence generated in recent years indicates that these two isoforms are also subject to expressional regulation. In view of the important biological functions of these …

LipopolysaccharidesGene isoformNitric Oxide Synthase Type IIITranscription GeneticNOS1Nitric Oxide Synthase Type IBiochemistryTranscription (biology)GeneticsTranscriptional regulationAnimalsHumansRNA MessengerGrowth SubstancesMolecular BiologyTranscription factorRegulation of gene expressionPolymorphism GeneticbiologyChemistryChromosome MappingLysophosphatidylcholinesNitric Oxide Synthase Type IIIEstrogensExonsCell biologyIsoenzymesLipoproteins LDLOxygenNitric oxide synthaseGene Expression Regulationbiology.proteinCytokinesNitric Oxide SynthaseGene DeletionBiotechnologyThe FASEB Journal
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Specific enrichment of 2-arachidonoyl-lysophosphatidylcholine in carotid atheroma plaque from type 2 diabetic patients

2016

IF 3.942; International audience; Background and aims: Diabetic patients are at high risk of stroke and coronary artery disease. Recent data suggest that arachidonic acid metabolism is altered in diabetic conditions and that these alterations contribute to accelerated atherosclerosis. Little is known about how these alterations affect the metabolism and the proportions of different lipid species within the atherosclerotic plaque. The aim of our study was to perform a targeted lipidomic analysis of human atherosclerotic lesions, with a specific focus on PUFA-containing lipid species, to reveal differences in the fatty-acid composition of plaque in diabetic patients compared with non-diabetic…

Male0301 basic medicineEndothelial lipasePathologymedicine.medical_treatmentCoronary Artery DiseaseCarotid endarterectomy030204 cardiovascular system & hematologyCohort StudiesCoronary artery diseasechemistry.chemical_compound0302 clinical medicineEndarterectomy CarotidLysophosphatidylcholineDiabetesMiddle Aged[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemPrognosisLipidsPlaque Atherosclerotic3. Good healthStrokeCholesterolArachidonic acidCholesteryl esterFemalelipids (amino acids peptides and proteins)Arachidonic acidCardiology and Cardiovascular Medicinemedicine.medical_specialtyContext (language use)Biology03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemDiabetes mellitusInternal medicinemedicineHumansAgedLysophosphatidylcholinesLipaseAtherosclerosismedicine.disease030104 developmental biologyAtheromaEndocrinologyDiabetes Mellitus Type 2chemistryMultivariate AnalysisEicosanoidsAtherosclerosis
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Lipidomic profiling identifies signatures of metabolic risk

2020

Background: Metabolic syndrome (MetS), the clustering of metabolic risk factors, is associated with cardiovascular disease risk. We sought to determine if dysregulation of the lipidome may contribute to metabolic risk factors. Methods: We measured 154 circulating lipid species in 658 participants from the Framingham Heart Study (FHS) using liquid chromatography-tandem mass spectrometry and tested for associations with obesity, dysglycemia, and dyslipidemia. Independent external validation was sought in three independent cohorts. Follow-up data from the FHS were used to test for lipid metabolites associated with longitudinal changes in metabolic risk factors. Results: Thirty-nine lipids were…

Male0301 basic medicineResearch paperdhSL dihydrosphingolipidBMI body mass indexlcsh:MedicineATHEROGENIC LIPOPROTEINSBioinformaticsFHS Framingham Heart StudyPC phosphatidylcholinePESA Progression of Early Subclinical Atherosclerosis0302 clinical medicineFramingham Heart StudyRisk FactorsSAFHS San Antonio Family Heart StudyLC-MS/MS liquid chromatography-tandem mass spectrometryMedicineLongitudinal StudiesMetabolic riskPLASMA SPHINGOLIPID METABOLISMPOPULATIONlcsh:R5-920education.field_of_studySPHINGOMYELINCE cholesteryl esterDysglycemiaGeneral MedicineMiddle AgedLipidomePS phosphatidylserineCardiovascular diseaseLipidsMetabolic syndrome3. Good healthCARDIOVASCULAR-DISEASE030220 oncology & carcinogenesisHEARTMetS metabolic syndromeFemaleDisease SusceptibilityLGPL lysoglycerophospholipidSL sphingolipidlcsh:Medicine (General)LPE lysophosphatidylethanolamineAdultFDR false discovery rateTAG triacylglycerolPopulationCer ceramideCVD cardiovascular diseasePE phosphatidylethanolamineDENSITY-LIPOPROTEINRisk AssessmentGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAnimalsHumanseducationT2DM type II diabetes mellitusAgedLPC lysophosphatidylcholineSM sphingomyelinbusiness.industryCERAMIDElcsh:RHDL-C High density lipoprotein cholesterolBiomarkerLipid Metabolismmedicine.diseaseObesitySphingolipidCross-Sectional Studies030104 developmental biologyDyslipidemiaERF Erasmus Family StudyLipidomicsMetabolic syndromeINDUCED INSULIN-RESISTANCEbusinessDAG diacylglycerolBody mass indexBiomarkersDyslipidemiaMRM multiple reaction monitoringFASTING GLUCOSE
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Long-term moderate magnesium-deficient diet shows relationships between blood pressure, inflammation and oxidant stress defense in aging rats

2006

International audience; Epidemiological and experimental studies have indicated a relationship among aging, dietary Mg, inflammatory stress, and cardiovascular disease. Our aim in the present study was to investigate possible links between dietary Mg, oxidant stress parameters, and inflammatory status with aging in rats. We designed a long-term study in which rats were fed for 22 months with moderately deficient (150 mg/kg), standard (800 mg/kg), or supplemented (3200 mg/kg) Mg diets. Comparisons were made with young rats fed with the same diets for 1 month. Compared to the standard and supplemented diets, the Mg-deficient diet significantly increased blood pressure, plasma interleukin-6, f…

MaleMESH: Inflammationmedicine.medical_specialtyMESH: RatsThiobarbituric acid[SDV]Life Sciences [q-bio]Blood PressureInflammationMESH: Rats Sprague-Dawley030204 cardiovascular system & hematologymedicine.disease_causeFibrinogenBiochemistryRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)Internal medicinemedicineTBARSAnimalsMESH: Animals030304 developmental biologyInflammation2. Zero hunger0303 health sciencesMESH: Oxidative StressMESH: Blood Pressuremedicine.diseaseMESH: MaleHemolysisRats3. Good healthOxidative StressLysophosphatidylcholineBlood pressureEndocrinologychemistryImmunologymedicine.symptomMagnesium DeficiencyMESH: Magnesium DeficiencyOxidative stressmedicine.drugFree Radical Biology and Medicine
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Bilobalide, a constituent of Ginkgo biloba , inhibits NMDA-induced phospholipase A 2 activation and phospholipid breakdown in rat hippocampus

2000

In rat hippocampal slices superfused with magnesium-free buffer, glutamate (1 mM) caused the release of large amounts of choline due to phospholipid breakdown. This phenomenon was mimicked by N-methyl-D-aspartate (NMDA) in a calcium-sensitive manner and was blocked by NMDA receptor antagonists such as MK-801 and 7-chlorokynurenate. The NMDA-induced release of choline was not caused by activation of phospholipase D but was mediated by phospholipase A2 (PLA2) activation as the release of choline was accompanied by the formation of lyso-phosphatidylcholine (lyso-PC) and glycerophospho-choline (GPCh) and was blocked by 5-[2-(2-carboxyethyl)-4-dodecanoyl-3,5-dimethylpyrrol-1-yl]pentano ic acid, …

MaleMicrodialysisN-MethylaspartateMicrodialysisGlycineCyclopentanesPharmacologyHippocampal formationHippocampusReceptors N-Methyl-D-AspartatePhospholipases ACholinechemistry.chemical_compoundPhospholipase A2BilobalideSeizuresAnimalsCholineRats WistarFuransCells CulturedPhospholipidsPharmacologyPlants MedicinalDose-Response Relationship DrugbiologyPhospholipase DGlutamate receptorGinkgo bilobaLysophosphatidylcholinesGeneral MedicineGlycerylphosphorylcholineRatsEnzyme ActivationPhospholipases A2Ginkgolideschemistrybiology.proteinNMDA receptorDiterpenesNaunyn-Schmiedeberg's Archives of Pharmacology
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HACD1, a regulator of membrane composition and fluidity, promotes myoblast fusion and skeletal muscle growth

2015

International audience; The reduced diameter of skeletal myofibres is a hallmark of several congenital myopathies, yet the underlying cellular and molecular mechanisms remain elusive. In this study, we investigate the role of HACD1/PTPLA, which is involved in the elongation of the very long chain fatty acids, in muscle fibre formation. In humans and dogs, HACD1 deficiency leads to a congenital myopathy with fibre size disproportion associated with a generalized muscle weakness. Through analysis of HACD1-deficient Labradors, Hacd1-knockout mice, and Hacd1-deficient myoblasts, we provide evidence that HACD1 promotes myoblast fusion during muscle development and regeneration. We further demons…

Male[SPI.GPROC] Engineering Sciences [physics]/Chemical and Process EngineeringCellular differentiationGeneralized muscle weaknessBiologyMuscle Developmentcentronuclear myopathyCell LineMyoblasts03 medical and health scienceschemistry.chemical_compoundMyoblast fusionMice0302 clinical medicineDogsVLCFA[SDV.IDA]Life Sciences [q-bio]/Food engineeringGeneticsmedicineMyocyteAnimalsHumans[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringMUFACentronuclear myopathyMuscle SkeletalMolecular Biology030304 developmental biologyMice Knockout0303 health sciencesPTPLACell MembraneSkeletal muscleCell DifferentiationCell BiologyGeneral MedicineArticles[SDV.IDA] Life Sciences [q-bio]/Food engineeringmedicine.diseaseCongenital myopathyLysophosphatidylcholinemedicine.anatomical_structureLPCchemistryBiochemistryFemaleProtein Tyrosine Phosphatasescentronuclear myopathy;lpc;mufa;ptpla;vlcfa030217 neurology & neurosurgery
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Uptake and metabolism of [3H]choline by the rat phrenic nerve-hemidiaphragm preparation

1987

A whole nerve-muscle preparation (about 160 mg) or an end-plate preparation (about 25 mg) of the rat phrenic nerve-hemidiaphragm were incubated with [3H]choline, to investigate choline uptake and choline metabolism. Choline uptake was measured from the disappearance of choline from the incubation medium during the loading period and from the retention of tritium in the tissue after the loading and washout period. Based on the results obtained with both methods the end-plate preparation takes up three times as much choline than the whole nerve-muscle preparation or a small muscle strip that was cut outside the end-plate region and had a similar size as the end-plate preparation. Choline upta…

Malemedicine.medical_specialtyMetaboliteDiaphragmNeuromuscular JunctionPhospholipidIn Vitro TechniquesBiologyMotor EndplateNeuromuscular junctionCholinechemistry.chemical_compoundPhosphatidylcholineInternal medicinemedicineAnimalsCholinePhrenic nervePharmacologyRats Inbred StrainsHemicholinium 3General MedicineMetabolismMuscle DenervationRatsPhrenic NerveLysophosphatidylcholinemedicine.anatomical_structureEndocrinologychemistryNaunyn-Schmiedeberg's Archives of Pharmacology
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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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Alteration of DNA topoisomerase II activity during infection of H9 cells by human immunodeficiency virus type 1 in vitro: a target for potential ther…

1990

Infection of H9 cells with human immunodeficiency virus type 1 (HIV-1) was found to decrease the phosphorylation of DNA topoisomerase II during the initial phase of infection. Simultaneously, with a later overshoot of phosphorylation and the subsequent activation of DNA topoisomerase II, the production of HIV-1 started. Applying three new protein kinase C inhibitors from the class of O-alkylglycerophospholipids we demonstrated that inhibition of protein kinase C-mediated phosphorylation of DNA topoisomerase II resulted in an inhibition of HIV-1 production. Based on the differential effect of the two protein kinase C activators, phorbol ester and bryostatin, we conclude that phosphorylation …

T-LymphocytesMitogen-activated protein kinase kinaseIn Vitro TechniquesMAP2K7Cell LineLactonesVirologyAnimalsPhosphorylationProtein kinase AProtein kinase CProtein Kinase CPharmacologybiologyCyclin-dependent kinase 2LysophosphatidylcholinesRats Inbred StrainsDNA topoisomerase II activityBryostatinsProtein kinase RMolecular biologyRatsDNA Topoisomerases Type Ibiology.proteinHIV-1Tetradecanoylphorbol AcetateCyclin-dependent kinase 9Electrophoresis Polyacrylamide GelMacrolidesAntiviral research
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Involvement of Oxysterols and Lysophosphatidylcholine in the Oxidized LDL–Induced Impairment of Serum Albumin Synthesis by HEPG2 Cells

2000

Abstract —Oxidized low density lipoproteins (Ox-LDLs) are increasingly thought to be a key element in atherogenesis. We have previously reported that serum albumin has important antioxidant properties and that a reduced synthesis of albumin may represent a crucial point in the overall antioxidant defense. In the present work, we aimed at determining whether Ox-LDL could modulate albumin synthesis in cultured human hepatocytes (HepG2 cells). With the use of enzyme immunoassay and radiolabeled leucine incorporation followed by specific immunoprecipitation, Ox-LDL was found to lead to a dose-dependent decrease in albumin secretion. Moreover, the protein synthesis and mRNA levels were decrease…

medicine.medical_specialtyTime FactorsAntioxidantmedicine.medical_treatmentHypercholesterolemiaSerum albuminDown-RegulationTritiumAntioxidantsLipid peroxidationchemistry.chemical_compoundLeucineInternal medicineDiabetes MellitusTumor Cells CulturedmedicineHumansRNA MessengerKetocholesterolsSerum AlbuminDose-Response Relationship DrugbiologyChemistryAlbuminLysophosphatidylcholinesBiological activityHydroxycholesterolsIn vitroLipoproteins LDLEndocrinologyLysophosphatidylcholinemedicine.anatomical_structureGene Expression RegulationLiverBiochemistryHepatocytebiology.proteinlipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineArteriosclerosis, Thrombosis, and Vascular Biology
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