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47 results on '"HUMAN ATHEROSCLEROTIC PLAQUE"'

10. Oxidized LDL-Induced Apoptosis

Author

Benoist, Hervé, Salvayre, Robert, Nègre-Salvayre, Anne, Harris, J. Robin, editor, Hilderson, H. J., editor, Biswas, B. B., editor, Quinn, Peter J., editor, and Kagan, Valerian E., editor

Published
2002
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36. Glucosylceramide modifies the LPS-induced inflammatory response in macrophages and the orientation of the LPS/TLR4 complex in silico

Author

Mobarak, Edouard, Håversen, Liliana, Manna, Moutusi, Rutberg, Mikael, Levin, Malin, Perkins, Rosie, Rog, Tomasz, Vattulainen, Ilpo, Borén, Jan, Department of Physics, Tampere University, Physics, and Research group: Biological Physics and Soft Matter

Subjects
Lipopolysaccharides, Male, Protein Conformation, alpha-Helical, STRUCTURAL BASIS, MOLECULAR-DYNAMICS SIMULATIONS, Primary Cell Culture, Lymphocyte Antigen 96, Gene Expression, SIGNAL-TRANSDUCTION, lcsh:Medicine, Molecular Dynamics Simulation, Glucosylceramides, ATOMISTIC SIMULATIONS, 114 Physical sciences, Article, Mice, Animals, Humans, Protein Interaction Domains and Motifs, lcsh:Science, ATOM FORCE-FIELD, TOLL-LIKE RECEPTORS, Binding Sites, Macrophage Colony-Stimulating Factor, Macrophages, Myelin and Lymphocyte-Associated Proteolipid Proteins, Cell Membrane, lcsh:R, Cell Differentiation, Hematopoietic Stem Cells, Mice, Inbred C57BL, Toll-Like Receptor 4, SWISS-MODEL, LIPID RAFTS, HEK293 Cells, TLR4-MD-2 COMPLEX, Glucosyltransferases, HUMAN ATHEROSCLEROTIC PLAQUE, 1182 Biochemistry, cell and molecular biology, Protein Conformation, beta-Strand, lipids (amino acids, peptides, and proteins), lcsh:Q, Protein Binding, Signal Transduction
Abstract

Toll-like receptor 4 (TLR4) is activated by bacterial lipopolysaccharide (LPS), which drives the production of proinflammatory cytokines. Earlier studies have indicated that cholesterol- and glycosphingolipid-rich subregions of the plasma membrane (lipid domains) are important for TLR4-mediated signaling. We report that inhibition of glucosylceramide (GluCer) synthase, which resulted in decreased concentrations of the glycosphingolipid GluCer in lipid domains, reduced the LPS-induced inflammatory response in both mouse and human macrophages. Atomistic molecular dynamics simulations of the TLR4 dimer complex (with and without LPS in its MD-2 binding pockets) in membranes (in the presence and absence of GluCer) showed that: (1) LPS induced a tilted orientation of TLR4 and increased dimer integrity; (2) GluCer did not affect the integrity of the LPS/TLR4 dimer but reduced the LPS-induced tilt; and (3) GluCer increased electrostatic interactions between the membrane and the TLR4 extracellular domain, which could potentially modulate the tilt. We also showed that GCS inhibition reduced the interaction between TLR4 and the intracellular adaptor protein Mal. We conclude that the GluCer-induced effects on LPS/TLR4 orientation may influence the signaling capabilities of the LPS/TLR4 complex by affecting its interaction with downstream signaling proteins. publishedVersion

Published
2018

37. Identification of macrophages and smooth muscle cells with monoclonal antibodies in the human atherosclerotic plaque.

Author

Roessner, A., Herrera, A., Höning, H., Vollmer, E., Zwadlo, G., Schürmann, R., Sorg, C., and Grundmann, E.

Abstract

Sections of human atherosclerotic plaques, obtained from 21 autopsy cases with various degrees of atherosclerosis, were stained with the indirect immunoperoxidase technique using specific monoclonal antibodies against macrophages and smooth muscle cells. Distinctive results were found in differing stages: Single blood monocytes were observed in diffuse intimal thickening and the foam cells seen in fatty streaks were mostly identified as mature tissue macrophages, while only very few blood monocytes were present. The spindle cells observed in fibroelastic plaques showed positive reactions to antibodies against desmin, which points to their derivation from smooth muscle cells, whereas only a few macrophage-derived foam cells were seen in these lesions. In the complicated lesions the majority of foam cells were macrophage-derived, but there was also a small number of foam cells positive to antibodies against desmin, suggesting a smooth muscle cell derivation. - Our results confirm that in human atherosclerotic plaques the majority of the foam cells are obviously macrophage-derived, which emphasizes the important role of macrophages in the morphogenesis of these lesions. [ABSTRACT FROM AUTHOR]

Published
1987
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45. Elevated remnant-like particle cholesterol concentration: a characteristic feature of the atherogenic lipoprotein phenotype

Author

Geesje M. Dallinga-Thie, Th.B. Twickler, M. J. Chapman, and J. S. Cohn

Subjects
Very low-density lipoprotein, medicine.medical_specialty, Arteriosclerosis, FAMILIAL COMBINED HYPERLIPIDEMIA, Lipoproteins, LOW-DENSITY-LIPOPROTEIN, APO A-I, TYPE-2 DIABETES-MELLITUS, Coronary Disease, Hyperlipidemias, ISCHEMIC-HEART-DISEASE, INTIMA-MEDIA THICKNESS, chemistry.chemical_compound, Risk Factors, Physiology (medical), Internal medicine, Medicine, Humans, Triglycerides, Hypolipidemic Agents, Intermediate-density lipoprotein, Lipoprotein lipase, business.industry, Cholesterol, Endocrinology and reproduction [UMCN 5.2], HORMONE REPLACEMENT THERAPY, Endocrinology, Phenotype, chemistry, Intima-media thickness, Low-density lipoprotein, HUMAN ATHEROSCLEROTIC PLAQUE, CORONARY-ARTERY-DISEASE, lipids (amino acids, peptides, and proteins), Hepatic lipase, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Cardiology and Cardiovascular Medicine, business, TRIGLYCERIDE-RICH LIPOPROTEINS, Biomarkers, Lipoprotein
Abstract

Patients at increased risk of coronary artery disease (CAD) frequently exhibit an atherogenic lipoprotein phenotype characterized by elevated plasma levels of both triglyceride-rich lipoproteins (TRL) and small, dense LDL and low concentrations of HDL cholesterol. Recently, in a large observational study, the calculated non-HDL plasma cholesterol concentration (the sum of the cholesterol contents of LDL, intermediate-density lipoprotein [IDL], and very-low-density lipoprotein [VLDL]) was a stronger predictor of cardiovascular events than plasma cholesterol alone.1–3 Improvement in the predictability of CAD on inclusion of VLDL and IDL cholesterol emphasizes the proatherogenic nature of TRL and their remnant particles. The atherogenic lipoprotein phenotype has been defined by Austin et al4 as the presence of a predominance of small, dense LDL particles, elevated plasma triglyceride (TG) levels, and low plasma HDL cholesterol levels in the lipoprotein profile, which is associated with an approximately 3-fold increased risk of atherosclerotic disease.5–8 It is now commonly accepted that small, dense LDL particles are the products of the intravascular remodeling of TG-rich VLDL particles after interaction primarily with lipoprotein lipase, hepatic lipase, and cholesterol ester transfer protein9,10 (Figure). The atherogenic lipoprotein phenotype is strongly linked to obesity, insulin resistance, familial combined hyperlipidemia (FCHL), hypertension, and abnormalities in postprandial lipid metabolism.7,11,12 Epidemiological data from the Framingham study have already revealed that plasma TG concentration is an important independent risk indicator of CAD in women13; additional evidence supporting this observation was obtained by Yarnell et al14 in a 10-year follow-up study and confirmed by others.15,16 In the PROCAM (Prospective Cardiovascular Munster) study,17 this relationship was dependent on plasma HDL cholesterol concentration. Criqui et al,18 however, could not demonstrate an independent relationship between plasma TG and cardiovascular mortality in a North American population participating in the Lipid Research Clinics Follow-up. …

Published
2004

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