Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ultrastructure and the expression of cytoskeletal and contractile proteins were studied in the intimal cells of human coronary arteries (CA) taken at autopsy from 38 trauma victims aged 1 to 70 years. All intimal smooth muscle cells (SMC) of the CA from 2-4-year old children contained desmin, vimentin, myosin, and actin. In the normal intima of adolescents aged 14-16 years, only did some SMC contain desmin whereas in that of adults, they had no desmin, but expressed all other proteins. For example, some atherosclerotic plaques of CA exhibited desmin-positive SMC and smooth muscle myosin-free cells. The ultrastructure of SMC of atherosclerotic plaques showed profound polymorphism. In addition to typical SMC, the plaques displayed modified cells having a developed endoplasmic reticulum and Golgi complex. The fact that the atherosclerotic plaques have cells differing in ultrastructural features and protein expression, which is specific to an earlier period of the body development suggests phenotypic changes in the cells and the latter acquiring new functions that are of great significance in the pathogenesis of atherosclerosis.
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PMID:[Phenotype changes in smooth muscle cells of human coronary arteries during aging and during development of atherosclerosis]. 179 63

The internal mammary artery (IMA) is used widely in bypass grafting for coronary artery disease because of its resistance to atherosclerotic obstruction. Since there are no data on the ultrastructure of IMA or the phenotype of its smooth muscle cells (SMC), we studied the distal parts of left IMA obtained at the time of surgery from 14 coronary bypass patients, aged 43-67 years. Eight IMA were examined by transmission electron microscopy. The distribution of the cytoskeletal proteins actin, vimentin, and desmin in the intima-media of 6 IMA was studied by immunofluorescence microscopy, polyacrylamide gel electrophoresis, and two-dimensional gel electrophoresis. The intimas were very thin, from 3 to 32 microns. The thinnest regions contained no cells. Most intimal cells had the ultrastructural features of SMC; no foam cells were found. The majority of both intimal and medial SMC had a myofilament-rich phenotype. Cells reacting to antibodies of vimentin, desmin and alpha-actin were found in both intima and media. alpha-Actin formed 67% of all actin isoforms in the intima-medial extracts. Our study confirms ultrastructurally the reported scarcity of atherosclerosis in the human IMA and shows that the majority of SMC in the IMA of even severely atherosclerotic coronary bypass patients are both ultrastructurally and biochemically in a differentiated state, which agrees with their resistance to atherosclerosis.
Atherosclerosis 1989 Oct
PMID:Ultrastructural, immunochemical and electrophoretic study of smooth muscle cells in internal mammary arteries of patients undergoing coronary bypass surgery. 268 63

The Simpson atherectomy device used for the recanalization of severely stenosed peripheral arteries is able to collect plaque material which can be further characterized. This study reports histological, immunohistochemical and transmission electron microscopic findings on advanced human primary atherosclerotic plaques of peripheral arteries percutaneously removed by a Simpson atherectomy catheter. Material from stenosing plaques consisted of dense connective tissue with abundant amounts of concentrically arranged elastic fibers and lamellae. This meshwork contained numerous cells, often arranged in clusters and oriented with their longer axis parallel to the direction of blood flow. The vast majority of these cells could be easily identified as vimentin-positive and desmin-negative smooth muscle cells containing lipid deposits in the perinuclear region and numerous glycogen particles. Monocytes/macrophages were observed only very infrequently. Plaque tissue contained a range of smooth muscle cell phenotypes. Most of the cells were of an intermediate phenotype, i.e. sparsely filled with myofilament bundles at the cell periphery and a high amount of organelles such as mitochondria, rough endoplasmic reticulum and Golgi cisterns. An intact lining of pieces of intimal tissue with endothelial cells was not observed. Two-dimensional gel electrophoresis of plaque tissue showed the presence of alpha-, beta- and gamma-actin isoforms with a clear predominance of the beta-isoform.
Atherosclerosis 1989 Dec
PMID:Cell constitution and characteristics of human atherosclerotic plaques selectively removed by percutaneous atherectomy. 269 72

The cellular composition of human atherosclerotic plaques was analyzed by immunologic techniques. Plaques were removed from the internal carotid artery during surgery, and a panel of monoclonal antibodies was used to identify cell types. Macrophages stained by Anti-Leu-M3 were found throughout the plaque, particularly in the lipid core region, where 60% of the cells reacted with this antibody. T cells expressing the T3 antigen were most abundant in the fibrous cap, where they constituted 20% of the cell population. T cells were also isolated from the plaque and detected by a rosetting test; many of these T cells were activated, as indicated by the expression of HLA-DR. Other types of leukocytes were uncommon in the plaque. An antibody to the intermediate filament protein, desmin, was used as a marker for smooth muscle cells since some, but not all, vascular smooth muscle cells contain this protein. The desmin-positive cells were uncommon in the nonatherosclerotic intima but were more numerous in the plaque. In conclusion, atherosclerotic plaques are heterogeneous with respect to cellular composition. The smooth muscle cell dominates in the fibrous cap, which also contains many T cells; the lipid core is dominated by macrophages. We suggest that interactions between smooth muscle cells and blood-borne cells are important in the pathogenesis of atherosclerosis.
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PMID:Regional accumulations of T cells, macrophages, and smooth muscle cells in the human atherosclerotic plaque. 293 95

We investigated two monoclonal antibodies (MAbs) which recognize rabbit atherosclerotic tissues. In particular, one antibody, 2P1A2, is specific for rabbit aortic smooth muscle cells (RASMCs). We used RASMCs in primary culture to produce and screen MAbs directed towards the cell surface. The specificity of the described antibodies was tested on a battery of tissue cryosections of different origin (rabbit, rat and human) by immunological staining. 2P1A2 shows an exclusive immunolabeling for SMCs present inside rabbit atherosclerotic plaque. This MAb shows inside the fibrous plaque a staining similar to two other SMC-specific antibodies (anti-desmin and anti-alpha-actin). In an early stage of atherosclerosis, close to the internal elastic lamina, underlying a fibrous plaque, 2P1A2 detects some SMCs; in contrast, anti-desmin and anti-alpha-actin fail to stain such SMCs. This antibody may be therefore considered as directed specifically against SMCs in an activated state. The other antibody which we describe, 1PC1, stains a pericellular antigen expressed by cultured SMCs and shows a specificity for smooth muscle tissues. 1PC1 MAb strongly stains the fibrous plaque of atherosclerotic rabbit aorta and the recognized epitope is present inside the aortic media. These two antibodies may be useful in the recognition of vascular SMCs during the atherosclerotic process.
Atherosclerosis 1988 Nov
PMID:Detection of atherosclerotic plaque with two monoclonal antibodies. 2P1A2 monoclonal antibody is specific for smooth muscle cells in atherosclerotic plaque. 306 71

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.
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PMID:Identification of macrophages and smooth muscle cells with monoclonal antibodies in the human atherosclerotic plaque. 312 17

Subendothelial cells (SEC) were obtained from the inner intimal layer of adult human aorta by collagenase treatment. SEC were identified in primary culture either as smooth muscle cells by staining with FITC-labeled antisera against human smooth muscle myosin or as macrophages, foam cells and contaminating endothelial cells by their uptake of malondialdehyde treated low density lipoproteins labeled with fluorescent dye 3,3'-dioctadecylindocarbocyanine. Between 1 and 5 days in culture, along with smooth muscle cells (SMC, 38-82%), endothelial cells (0-9%), macrophages and foam cells (2-32%), one more type of cell was found. This cell type resembled SMC in size and shape, but was not stained by antisera to SMC myosin. By ultrastructural criteria these cells were characterized as modulated SMC for they contained prominent rough endoplastic reticulum and Golgi complex together with basement membrane and a large number of plasmalemmal vesicles. Like SMC they reacted with phalloidin and were stained by anti-vimentin but not by anti-desmin monoclonal antibodies. The proportion of such cells varied from 5 to 33% of total cell number and increased in parallel to macrophages and foam cells in vessels with well developed atherosclerotic lesions. We conclude that the applied technique may be used for identification of cultured vascular cells including modulated SMC.
Atherosclerosis 1988 May
PMID:Identification of intimal subendothelial cells from human aorta in primary culture. 313 80

The phenotype of smooth muscle cells (SMCs) in the aortic media of 7 human fetuses (14-20 weeks of gestation) was examined with transmission electron microscopy, immunofluorescence microscopy, and gel electrophoresis of the cytoskeletal and cytocontractile proteins. Ultrastructurally, virtually all medial cells were identified as SMCs having a poorly differentiated phenotype with a cytoplasm rich in rough endoplasmic reticulum and organelles, and with only a few myofilaments. All medial cells stained intensely with antibodies to vimentin, but only in a 20-week-old fetus could we find a few SMCs staining with antibodies to desmin. Nor was desmin detectable with SDS gel electrophoresis followed by immunoblotting, while clear bands corresponding to vimentin, myosin, and actin were present. In isoelectric focusing and two-dimensional gel electrophoresis beta-actin was the most prominent of the 3 actin isoforms in all cases. The present results show that SMCs in the media of fetal human aorta have a poorly differentiated phenotype, which morphologically and biochemically resembles that previously described in the aorta of fetal and newborn rat, in the arterial intima after endothelial injury, in atherosclerotic lesions, and after spontaneous modulation of medial SMCs in culture.
Atherosclerosis 1988 Nov
PMID:Characterization of the phenotype of smooth muscle cells in human fetal aorta on the basis of ultrastructure, immunofluorescence, and the composition of cytoskeletal and cytocontractile proteins. 321 79

The aortic walls of patients with abdominal aortic aneurysms (AAA) and of healthy controls were examined for elastin, collagen I and III, and the intermediate filament proteins desmin and vimentin by immunohistochemical, enzyme histochemical, and routine histological techniques. The morphology of the aneurysmatic walls varied considerably from case to case, but many pathological changes were seen in all cases, e.g., extensive atherosclerotic plaques in the intima, prominent alterations in amount and organization of the elastic lamellae in the media, and an increase of connective tissue. Both collagen I and III were present in all the aneurysmatic walls. The smooth muscle cells in all the aortic walls showed a marked heterogeneity with respect to the morphological appearance, the enzyme histochemical features, and the content of desmin and vimentin. Vimentin occurred in some intimal, medial muscle, and adventitial cells of both the controls and the AAA patients. Desmin occurred in some of the intimal, medial, and adventitial muscle cells of both the controls and the AAA patients. All the cells with desmin in the intima and media also contained vimentin. Thus, smooth muscle cells in the walls of both the normal human abdominal aorta and aneurysms contained either vimentin, desmin, or both. This variability may be explained by the presence of different phenotypes of smooth muscle cells and could be of significance for the development of atherosclerosis and aneurysms. Of special interest was the finding that 5 of the 24 AAA patients studied had blood relatives with the same disease, suggesting a hereditary influence. However, no systematic differences between the morphological appearance of the aneurysmatic walls in familial and nonfamilial AAA could be detected.
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PMID:Abdominal aortic aneurysms: distribution of elastin, collagen I and III, and intermediate filament proteins desmin and vimentin--a comparison of familial and nonfamilial aneurysms. 353 8

A large proportion of the cells of the human atherosclerotic plaque is assumed to be derived from medial smooth muscle cells. In contrast to these, the cells of the plaque have the capacity to accumulate lipid, and they also proliferate at a higher rate than medial cells. It has therefore been suggested that smooth muscle cells undergo a change of phenotype during atherogenesis, but there has been no evidence for such a change on the molecular level. We have now analyzed carotid artery plaques using a battery of antibodies against cell surface and cytoskeletal antigens, and found that most of the cells express the class II transplantation antigen (Ia antigen) HLA-DR. Also, the beta chain of HLA-DR was detected by immunoblotting of plaque extracts with the OKIa1 monoclonal antibody. HLA-DR is normally present on cells of the immune system, but only 60% of the DR-positive cells of the plaque reacted with monoclonal antibodies specific for macrophages and lymphocytes. Many of the remaining DR-positive cells contained the muscle-specific intermediate filament protein, desmin. This indicates that smooth muscle cells of atherosclerotic plaques express DR antigen. In contrast, very few DR-positive cells were found in normal human arteries. This suggests that expression of class II antigen is part of a phenotypic change in smooth muscle cells in atherosclerosis.
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PMID:Expression of class II transplantation antigen on vascular smooth muscle cells in human atherosclerosis. 389 17


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