11/13. Ultrastructure of experimental coronary artery atherosclerosis in cynomolgus macaques. A comparison with the lesions of other primates.We studied the ultrastructure of the left anterior descending coronary artery in 6 female cynomolgus macaques fed atherogenic food containing 0.5% cholesterol for 6 months, and in 2 female cynomolgus macaques that had received food low in cholesterol. animals given the atherogenic food had coronary artery lesions of a characteristic two-level architecture consisting of a lipid-poor upper cap, and of a lipid-rich lower core. The cap consisted of layers of smooth muscle cells that were rich in rough endoplasmic reticulum and contained few myofilaments and relatively few lipid droplet inclusions. The core consisted mainly of macrophages overloaded with droplet inclusions (macrophage foam cells), droplet-laden smooth muscle cells, and extracellular lipid and cell debris. Some macrophage foam cells were in mitosis. The largest lipid cores contained multinucleate giant cells with large intracellular crystal clefts. Dead macrophage foam cells were the source of the extracellular lipid and debris particles. Intimal cores often extended into the adjacent media. The adventitia was involved in the intima-media lesions in 3 of the animals. Compared with the coronary artery lesions of rhesus macaques and patas monkeys given similar atherogenic diets, cynomolgus monkey lesions were morphologically closer to human atherosclerotic plaques with respect to their stratification into a cap and a core.- - - - - - - - - - ranking = 1keywords = macrophage (Clic here for more details about this article) |
12/13. Pseudo type III dyslipoproteinemia is associated with normal fibroblast lipoprotein receptor activity.Pseudo type III (PT-III) dyslipoproteinemia is characterized by a plasma accumulation of triglyceride-rich lipoproteins (TRL) and their remnants. It mimics type III, but its etiology can not be ascribed to a genetic apo E defect. In order to determine whether PT-III is associated with a genetic lipoprotein receptor abnormality, we have measured (in cultured fibroblasts from affected and nonaffected individuals) the in vitro activity of three lipoprotein receptors which are implicated in the catabolism of TRL, namely the low-density lipoprotein receptor (LDL-R), the lipoprotein receptor-related protein (LRP) and the lipolysis-stimulated receptor (LSR). Specific cell association and degradation of 125I-LDL by LDL-R-upregulated PT-III fibroblasts was not significantly different from that of control cells (103 /- 10% and 98 /- 17% of controls; 20 microg/ml 125I-LDL). Specific cell association and degradation of rabbit 125I-beta-VLDL was also not significantly different. LRP activity was assessed by measuring the ability of PT-III and control cells to bind three different LRP ligands: activated alpha2-macroglobulin (alpha2M-MA), lactoferrin and apo E-enriched rabbit beta-VLDL. No significant differences were observed (24.0 /- 2.1 vs. 23.4 /- 5.7 fmol/mg for 5 nM of 125I-alpha2M-MA; 4.8 /- 0.3 vs. 5.2 /- 1.3 microg/mg for 20 microg/ml of 125I-lactoferrin; 319.4 /- 51.2 vs. 309.5 /- 23.2 ng/mg for 5 microg/ml of 125I-beta-VLDL, PT-III vs. control, respectively). LSR activity, as assessed by the cell association or degradation of 125I-LDL by fibroblasts in the presence of 0.5 mM oleate and human leptin, was also not different. No evidence was obtained for deficient cellular recognition of PT-III TRL (d < 1.006 g/ml) by normal human fibroblasts or mouse macrophages. These results suggest that PT-III dyslipoproteinemia is not due to an accumulation in plasma of poorly recognized TRL, nor due to a genetic defect in LDL-R, LRP or LSR.- - - - - - - - - - ranking = 0.25keywords = macrophage (Clic here for more details about this article) |
13/13. Restricted usage of T-cell receptor Valpha-Vbeta genes in infiltrating cells in the aortic tissue of a patient with atherosclerotic aortic aneurysm.We report a rare case of an atherosclerotic aortic aneurysm with lymphocyte infiltration in which T-cell receptor (TCR) Valpha as well as Vbeta gene usage was restricted. Immunohistochemical studies showed that the infiltrating cells mainly consisted of macrophages, natural killer (NK) cells, cytotoxic T lymphocytes (CTLs) and T-helper (Th) cells, and that there were almost no infiltrating delta T lymphocytes, and human leukocyte antigen (HLA) class I and 65-kD heat-shock protein (HSP-65) was not strongly expressed in the aortic tissue. Although the immunohistochemical data were consistent with an ordinary atherosclerotic aortic aneurysm, in which TCR Valpha-Vbeta gene usage is known to be polyclonal, the restricted TCR gene usage suggests that a certain autoimmune mechanism was involved in the pathogenesis of this case similar to Takayasu's arteritis, in which massive infiltration of delta T lymphocytes and strong expression of HSP-65 in the aortic tissue are characteristic.- - - - - - - - - - ranking = 0.25keywords = macrophage (Clic here for more details about this article) |
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