Search results for "Foam cell"

showing 10 items of 20 documents

Human Oxidation-Specific Antibodies Reduce Foam Cell Formation and Atherosclerosis Progression

2011

ObjectivesWe sought to assess the in vivo importance of scavenger receptor (SR)–mediated uptake of oxidized low-density lipoprotein (OxLDL) in atherogenesis and to test the efficacy of human antibody IK17-Fab or IK17 single-chain Fv fragment (IK17-scFv), which lacks immunologic properties of intact antibodies other than the ability to inhibit uptake of OxLDL by macrophages, to inhibit atherosclerosis.BackgroundThe unregulated uptake of OxLDL by macrophage SR contributes to foam cell formation, but the importance of this pathway in vivo is uncertain.MethodsCholesterol-fed low-density lipoprotein receptor knockout (LDLR−/−) mice were treated with intraperitoneal infusion of human IK17-Fab (2.…

MaleoxidationGenetic enhancementGreen Fluorescent Proteins030204 cardiovascular system & hematologymedicine.disease_causeArticleAdenoviridaeMice03 medical and health sciences0302 clinical medicineIn vivoAnimalsHumansantibodiesMedicineScavenger receptorReceptorImmunoglobulin Fragments030304 developmental biologyFoam cellHomeodomain ProteinsMice Knockout0303 health sciencesbiologybusiness.industryMacrophagesscavenger receptorsgene therapyRecombinant Proteins3. Good healthLipoproteins LDLMice Inbred C57BLAdenoviridaeReceptors LDLImmunologyDisease ProgressionCancer researchbiology.proteinlipids (amino acids peptides and proteins)atherosclerosisAntibodyCardiology and Cardiovascular MedicinebusinessFoam CellsLipoproteinJournal of the American College of Cardiology
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Deficient p27 Phosphorylation at Serine 10 Increases Macrophage Foam Cell Formation and Aggravates Atherosclerosis Through a Proliferation-Independen…

2011

OBJECTIVE: Genetic ablation of the growth suppressor p27(Kip1) (p27) in the mouse aggravates atherosclerosis coinciding with enhanced arterial cell proliferation. However, it is unknown whether molecular mechanisms that limit p27's protective function contribute to atherosclerosis development and whether p27 exerts proliferation-independent activities in the arterial wall. This study aims to provide insight into both questions by investigating the role in atherosclerosis of p27 phosphorylation at serine 10 (p27-phospho-Ser10), a major posttranslational modification of this protein. METHODS AND RESULTS: Immunoblotting studies revealed a marked reduction in p27-phospho-Ser10 in atheroscleroti…

Malerho GTP-Binding ProteinsRHOAMoesinMiceApolipoproteins ERadixinSerinemedicineAnimalsHumansProtein phosphorylationPhosphorylationProtein kinase ACell ProliferationFoam cellMice Knockoutrho-Associated KinasesbiologyArteriesAtherosclerosismedicine.diseaseCell biologyMice Inbred C57BLDisease Models AnimalAtheromaCase-Control StudiesImmunologyDisease Progressionbiology.proteinPhosphorylationFemalerhoA GTP-Binding ProteinCardiology and Cardiovascular MedicineCyclin-Dependent Kinase Inhibitor p27Foam CellsSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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Verruciform xanthoma located in anterior gingiva

2010

Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:24:39Z No. of bitstreams: 0Bitstream added on 2014-05-27T14:46:45Z : No. of bitstreams: 1 2-s2.0-84865074614.pdf: 383535 bytes, checksum: 78e85eebb99986f003c26c99375b0a62 (MD5) Made available in DSpace on 2014-05-27T11:24:39Z (GMT). No. of bitstreams: 0 Previous issue date: 2010-04-01 Verruciform xanthoma (VX) is a relatively rare benign lesion and oral predominantly, which occasionally affects skin and genital mucosa. It appears as a papule or single plaque showing a verrucous or papillomatous aspect, with variable color from reddish pink to gray. In majority of oral cases, it affects gingiva and alv…

MouthPathologymedicine.medical_specialtybusiness.industryOdontologíaPapule:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseCiencias de la saludLesionDermal papillaemedicine.anatomical_structureConcomitantUNESCO::CIENCIAS MÉDICASXanthomatosismedicineEtiologySex organmedicine.symptomFoam cellsbusinessGeneral DentistryAlveolar mucosaVerruciform xanthomaJournal of Clinical and Experimental Dentistry
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A novel in vitro model for the study of plaque development in atherosclerosis

2006

SummaryFor the study of atherogenesis in vitro, coculture systems have been devised, in which two or more cell types can be cultured in close contact to each other. Herein, we describe a novel in vitro model that aims at the simulation of the morphology ofa normal muscular artery allowing for the study of the initial events in atherosclerosis. Usinga modified fibrin gel as a scaffold for the coculture of endothelial cells (ECs) and smooth muscle cells (SMCs), we generated an autologous in vitro model with a multilayer growth of SMCs (intima-like structure) covered by an endothelium. The production of extracellular matrix (ECM) could be visualized histologically and verified by (i) ascorbic-…

Pathologymedicine.medical_specialtyTime FactorsEndotheliumCellular differentiationMyocytes Smooth MuscleMonocytesMuscle Smooth VascularCell LineExtracellular matrixCell MovementLamininCell AdhesionmedicineHumansFoam cellFibrinDose-Response Relationship Drugbiologybusiness.industryEndothelial CellsCell DifferentiationHematologyAtherosclerosisCoculture TechniquesIn vitroExtracellular MatrixCell biologyLipoproteins LDLmedicine.anatomical_structureCell culturebiology.proteinbusinessGelsFoam CellsLipoproteinThrombosis and Haemostasis
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Enzymatically modified LDL induces cathepsin H in human monocytes: potential relevance in early atherogenesis.

2003

Objective—Modification with proteases and cholesterylesterase transforms LDL to a moiety that resembles lipoproteins isolated from atherosclerotic lesions and possesses atherogenic properties. To identify changes in monocyte-derived foam cells laden with enzymatically modified LDL (E-LDL), we compared patterns of the most abundant transcripts in these cells after incubation with LDL or E-LDL.Methods and Results—Serial analyses of gene expression (SAGE) libraries were constructed from human monocytes after treatment with LDL or E-LDL. Several tags were differentially expressed in LDL-treated versus E-LDL–treated cells, whereby marked selective induction by E-LDL of cathepsin H was conspicuou…

ProteasesCathepsin HCoronary Artery DiseaseBiologyCathepsin HCathepsin L1medicineMacrophageHumansFoam cellGene LibraryCathepsinMonocyteGene Expression ProfilingColocalizationSterol EsteraseMolecular biologyCathepsinsLipoproteins LDLCysteine Endopeptidasesmedicine.anatomical_structureCholesterolBiochemistryGene Expression Regulationlipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineFoam CellsArteriosclerosis, thrombosis, and vascular biology
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A029 Identification of polymorphisms in the gene encoding secreted phospholipase A2 group X and study of their role in coronary artery disease. The a…

2009

Human secreted phospholipases A2 (sPLA2s) represent novel attractive therapeutic targets and biomarkers in coronary artery diseases (CAD). We have shown that human Group X sPLA2 (hGX sPLA2) is present in atherosclerotic lesions and that hGX sPLA2 modified LDL induces foam cell formation. To elucidate whether hGX sPLA2 has a causative role in CAD we have screened the human PLA2G10 gene to identify frequent polymorphisms, and we have examined their possible association with cardiovascular end-points and intermediate inflammatory phenotypes in a large prospective study of patients with CAD (the AtheroGene study). Although no significant association was found between the various polymorphisms i…

Untranslated regionPathologymedicine.medical_specialtybiologybusiness.industryGeneral Medicinemedicine.diseasePhenotypeCoronary artery diseasePhospholipase A2Cancer researchbiology.proteinMedicineMissense mutationAlleleCardiology and Cardiovascular MedicinebusinessGeneFoam cellArchives of Cardiovascular Diseases
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On the pathogenesis of atherosclerosis: enzymatic transformation of human low density lipoprotein to an atherogenic moiety.

1995

Combined treatment with trypsin, cholesterol esterase, and neuraminidase transforms LDL, but not HDL or VLDL, to particles with properties akin to those of lipid extracted from atherosclerotic lesions. Single or double enzyme modifications, or treatment with phospholipase C, or simple vortexing are ineffective. Triple enzyme treatment disrupts the ordered and uniform structure of LDL particles, and gives rise to the formation of inhomogeneous lipid droplets 10-200 nm in diameter with a pronounced net negative charge, but lacking significant amounts of oxidized lipid. Enzymatically modified LDL (E-LDL), but not oxidatively modified LDL (ox-LDL), is endowed with potent complement-activating c…

Very low-density lipoproteinArteriosclerosisImmunologyNeuraminidaseComplement Membrane Attack Complexchemistry.chemical_compoundLipid dropletmedicineExtracellularImmunology and AllergyHumansTrypsinReceptors ImmunologicComplement ActivationGlycoproteinsReceptors Lipoproteinchemistry.chemical_classificationReceptors ScavengerPhospholipase CCholesterolMacrophagesMembrane ProteinsComplement C3Complement System ProteinsArticlesScavenger Receptors Class BSterol EsteraseTrypsinLipid MetabolismLipoproteins LDLEnzymechemistryBiochemistryLow-density lipoproteinlipids (amino acids peptides and proteins)medicine.drugFoam CellsThe Journal of experimental medicine
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Pathogenesis of Atherosclerosis: The Alternative Hypothesis

1998

The concept that oxidation is the major single event underlying the transformation of LDL to a proinflammatory molecule dominates the world literature. An alternative hypothesis on the pathogenesis of atherosclerosis will be presented here. We have found that nonoxidative, enzymatic modification of LDL with ubiquitous enzymes also transforms the molecule to an atherogenic moiety. Enzymatically altered LDL (E-LDL) shares major properties in common with lipoproteins that have been isolated from atherosclerotic lesions. It activates complement and is recognized by a scavenger receptor on human macrophages, thus inducing foam cell formation. Uptake of E-LDL is accompanied by induction of MCP−1 …

biologybusiness.industryComplement systemCell biologyProinflammatory cytokinePathogenesisImmunologybiology.proteinExtracellularMedicinelipids (amino acids peptides and proteins)Radiology Nuclear Medicine and imagingSecretionScavenger receptorAntibodyCardiology and Cardiovascular MedicinebusinessFoam cellJournal of Interventional Cardiology
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Complement C6 deficiency protects against diet-induced atherosclerosis in rabbits.

1998

Abstract —Low-density lipoprotein (LDL) can be transformed to an atherogenic moiety by nonoxidative, enzymatic degradation. Enzymatically degraded LDL induces macrophage foam cell formation, provokes release of cytokines, and also activates complement. To determine whether complement activation may contribute to atherogenesis, 6 pairs of homozygous C6-deficient rabbits and their non–C6-deficient heterozygous siblings were fed a cholesterol-rich diet for 14 weeks. Cholesterol levels and plasma lipoprotein profiles of the animals in the C6-competent and C6-deficient groups did not significantly differ, and the high density lipoprotein and LDL cholesterol ratios at the end of the experiment w…

medicine.medical_specialtyHeterozygoteArteriosclerosisBiologyPathogenesisCholesterol Dietarychemistry.chemical_compoundHigh-density lipoproteinInternal medicinemedicine.arterymedicineMacrophageAnimalsComplement ActivationFoam cellAortaCholesterolHomozygoteComplement systemComplement C6EndocrinologychemistryImmunologyDiet AtherogenicRabbitsCardiology and Cardiovascular MedicineLipoproteinArteriosclerosis, thrombosis, and vascular biology
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Bisphosphonates and atherosclerosis: why?

2005

The increasing knowledge on bone calcification processes has revealed some similarities with vascular tissue, where calcifications of arteries and cardiac valves contribute to several cardiovascular problems, such as heart failure, systolic hypertension, and myocardial and peripheral ischemic disease. Bisphosphonates have been used extensively for over two decades for the treatment of diseases associated with excessive bone resorption, i.e., osteoporosis, osteolytic bone metastasis, hypercalcemia and Paget’s disease, by blocking osteoclastic function. Etidronate, pamidronate and clodronate has been shown to inhibit the development of experimental atherosclerosis, and proposed mechanisms fo…

medicine.medical_specialtyOsteoporosisMevalonic AcidApoptosisDisease030204 cardiovascular system & hematologyBone resorption03 medical and health sciences0302 clinical medicineRheumatologyCalcinosisInternal medicinemedicineHumansBone ResorptionFoam cell030203 arthritis & rheumatologyDiphosphonatesMolecular Structurebusiness.industryMacrophagesBone metastasisCalcinosismedicine.diseaseAtherosclerosisArterial calcificationEndocrinologyCholesterolHeart failureCancer researchbusinessLupus
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