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)

Connective tissue composition of aortas from several non-human primate species has been studied in an effort to relate collagen, elastin, ang glycosaminoglycan (GAG) content to species susceptibility to atherosclerosis. Among the species studied the baboon contained the highest content of GAG in the aorta. While the distribution of individual GAG varied from species to species, heparan sulfate (HS) was the highest GAG in aortas from most of the species. The ratio of HS to chondroitin sulfates (CS) plus dermatan sulfate (DS) was lowest in the baboon, a species relatively less susceptible to atherosclerosis, and highest in the squirrel monkey, a very susceptible primate. If a relationship exists between HS to CS + DS ratio in the aorta and atherosclerosis, the primates can be arranged in the following decreasing order of susceptibility: squirrel, chimpanzee, stump-tailed, rhesus, African green, patas, baboon. In studies of other connective tissue components, the proportion of total collagen to elastin was found lowest in the baboon. Such observations emphasize the importance of connective tissue in the pathogenesis of atherosclerosis.
Atherosclerosis 1978 Jan
PMID:Connective tissue composition of aortas from non-human primates. A comparative study. 41 48

The authors examined neosynthesis of fiber proteins (scleroproteins) in the aorta of rats with genetic hypertonia and with experimental atherosclerosis after application of 3H-proline and 3H-lysine and subsequent determination of radioactivity of collagenous and elastic in the aortic wall. There was a great increase in incorporation a labelled precursors of collagen and elastin in the aorta of hypertonic and atherosclerotic animals in comparison with the control rats-a manifestation of increased "de novo" synthesis of fiber proteins in rats with these arterial diseases. Furthermore the increased collagenosis dominated over that of elastogenesis. The irregularity in the activation of biosynthesis of both sclero-proteins in rats with hypertonia and atherosclerosis caused remodeling of macromolecular structure of the aretrial wall with a predominance of collagen over the remaining components of the connective tissue matrix. The resulting fibrosis of the arterial wall favoured the fixation of hypertonia and progression of atherosclerosis.
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PMID:[Arterial scleroproteins in atherosclerosis and hypertension (experimental studies)]. 43 8

The effects of experimental (dietary) atherosclerosis on arteries from racing greyhounds were studied. Measurements of pressure and external diameter were made on islated carotid and iliac arteries under active (norepinephrine, 5 microgram/ml) and passive (zero Ca2+ and 2 mM EGTA) smooth muscle conditions. Iliac arteries from diet-fed animals demonstrated substantial intimal lesions, but the carotid arteries were usually grossly involved. Arteries from atherosclerotic animals were stiffer during passive conditions, with the iliac arteries having the greater changes. In iliac arteries from treated animals, collagen and elastin contents were decreased, and the collagen-to-elastin ratio was increased; in carotid arteries from treated animals, elastin content was increased and the collagen-to-elastin ratio was decreased. The maximum range of control of arterial wall mechanics by smooth muscle was diminished in treated iliacs but unchanged in carotids. Both force development and constriction responses associated with smooth muscle activation were diminished in treated iliacs but unchanged in treated carotids. Mechanical properties of series elastic elements in treated iliacs were stiffer, but treated carotids were unchanged.
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PMID:Arterial wall properties and dietary atherosclerosis in the racing greyhound. 44 41

Elastin was extracted from human aortic plaque and adjacent grossly normal intima by the following methods: (1) 0.1 N NaOH at 100 degrees C, (2) hot NaOH and 0.2 M EDTA, (3) 5 M guanidine--HCl and collagenase, (4) guanidine--collagenase and dithioerythritol--urea--sodium dodecyl sulfate, (5) guanidine--collagenase and EDTA, (6) 10% NaCl and collagenase, and (7) NaCl--collagenase and EDTA. All elastin samples contained small amounts of carbohydrate and hydroxyproline. The lipid content of non-plaque intimal elastin samples was small (2--3%), whereas it increased to 4--6% in plaque intima. The lipid composition of elastin preparations varied significantly with the extraction procedure. Elastin from plaque intima contained significantly more cholesterol (50--60%) and less triglyceride and phospholipid than elastin of non-plaque intima (30--50% cholesterol). The contents of free and esterified cholesterol were comparable in all preparations. The main phospholipid in all samples was sphingomyelin, which comprised between 50 and 80% of the total phospholipid. Compared with NaOH-purified elastin, the other elastin samples were characterized by an increased phosphatidyl--choline content, while they all contained an almost equal amount of phosphatidylethanolamine. In elastin samples from plaque intima, the polar amino acids were increased, whereas cross-linking amino acids were decreased. The polarity and hydroxyproline content of elastin samples were slightly decreased after treatment with EDTA or dithioerythritol--urea--sodium dodecyl sulfate.
Atherosclerosis 1979 May
PMID:Elastin--lipid interaction action in the arterial wall. Part 1. Extraction of elastin from human aortic intima. 46 28

Detailed studies of aortas from 8 rabbits showed that serious artefacts occur if the aortas are pinned at their in vivo dimensions, rather than fixed at physiological pressure. In the pinned aortas, the proximal parts of the branches were pulled up onto the aortic wall. This was more pronounced for the large branches of the abdominal aorta than for the smaller intercostal branches. This artefact caused atherosclerotic lesions, which had developed at the origin of the branch, to appear as if they were entirely on the aortic wall. We found that a marked change in the elastin pattern was present at the origin of the branch; this can be used to mark the true origin of the branch. With the pressure technique we found that lesions had different shapes and locations at different branch points.
Atherosclerosis 1978 Sep
PMID:Artefacts of localization of atherosclerosis in pinned aortas. 70 94

Thoracic aortae of normal rabbits were perfused with pancreatic elastase in vitro at 37 degrees C and 70 mm Hg pressure in the presence or absence of elastin ligands previously shown to stimulate or inhibit the enzymatic degradation of elastin. Perfusion with elastase results in an average of 3.6 lamellae degraded, whereas addition of sodium linoleate before and during the perfusion with elastase increases this value to 7.9 (P less than 0.001). Conversely, perfusion with the cationic detergent, dodecyltrimethylammonium chloride, completely prevents the degradation of elastic lamellae by elastase. These effects do not reflect alterations of the intrinsic catalytic activity of elastase, but apparently indicate the formation of complexes between the elastin ligands and arterial elastic lamellae, as is consistent with prior studies indicating such interactions between fatty acids or detergents and purified elastin. These studies suggest that agents such as fatty acids may significantly alter the metabolic susceptibility of elastin in vivo and possibly contribute to the degradation of elastic lamellae seen in arteries with advanced atherosclerosis.
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PMID:A possible role for elastin ligands in the proteolytic degradation of arterial elastic lamellae in the rabbit. 75 37

A possibility is shown of obtaining sufficiently pure antigens (collagen, elastin, structural grycoproteids), with the help of a preparative chemical method, from the wall of aortas of rabbits, both healthy and "diseased", i.e. with atherosclerosis. Immunomorphological analysis showed that the immune sera obtained against antigens indicated above reacted only with structures of the affected vessels, no interaction with the wall of normal aortas being noted.
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PMID:[Isolation of immune serums against antigens of the aorta for immunomorphological study of experimental atherosclerosis]. 77 46

A method is presented for grinding and extracting very small samples of tough fibrous tissue from single atherosclerotic lesions of human aortas. Grinding to a powder was easily accomplished while the samples were frozen in liquid nitrogen in a porcelain micromortar. Extractions of the powder were made first in the mortar and then in tapered centrifuge tubes. Salt soluble, dodecyl sulfate--mercaptoethanol--urea soluble and hot alkali soluble fractions were obtained, in addition to a hot alkali insoluble elastin residue from each sample. Variation in the protein composition of 23 samples from the lumenal surface of the severely atherosclerotic aorta of a 58-year-old human male were determined. The proteins soluble in the buffered-saline and the dodecyl sulfate-urea soluble polypeptides from each sample were analyzed by dodecyl sulfate--acrylamide gel electrophoresis. The amino acid compositions of the insoluble elastin fractions were determined. The 5 grossly normal intima samples had very similar gel electrophoresis band patterns and amino acid compositions. The 3 samples of necrotic gruel had markedly different dodecyl sulfate--urea soluble polypeptides than either normal or calcified tissue; they also had elastin fractions whose amino acid compositions were unique in that they contained 10 times more serine than elastin fractions from grossly normal intima. The 3 calcified samples had less saline or dodecyl sulfate soluble protein than either grossly normal or necrotic gruel samples, and had very altered elastin fraction compositions characterized by much higher contents of hydroxylysine than grossly normal intima. The elastin fractions of necrotic gruel and calcified tissue samples had little or no isodesmosine or desmosine, suggesting that little of the elastin found in healthy aorta tissue was present.
Atherosclerosis 1977 Feb
PMID:Variation in proteins of single lesions from the intima of the aorta from a human patient with severe atherosclerosis. 83 51

The effect of permanent occlusion on the carotid artery of the rat was studied by light and by electron microscopy. A segment between two ligatures was examined at times from 2 minutes to 1 year. Between 2 and 15 minutes after occlusion, the red blood cells adjacent to the wall formed radially arranged rouleaux; within 24 hours the endothelium disappeared, while platelets (despite the lack of flow) accumulated against the denuded elastica. This behavior of formed blood elements may have been the result of electric forces (injury potential). By 3 days, undifferentiated cells were found lining the elastica interna or free in the lumen; they apparently were derived from medial smooth muscle.In the media, by 3 days some smooth muscle cells had become necrotic, while "undifferentiated" cells appeared; strong circumstantial evidence suggested that these were smooth muscle cells which had lost their specific characteristics and had thus become dedifferentiated (a phenomenon also known to occur in striated muscle cells); by 1 month they had matured into smooth muscle, but the media from then on contained fewer cells and more collagen than normal.In the lumen, the undifferentiated cells also matured into typical smooth muscle cells from 15 days onward, while collagen and elastin appeared between them. After 1 month these cells began to accumulate droplets of fat, which thereafter increased in number (at 6 months they were associated with cholesterol clefts) and then declined. This accumulation of fat in smooth muscle cells (also seen in atherosclerosis) was interesting because it occurred in the absence of blood flow.
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PMID:Effect of occlusion on large vessels. I. A study of the rat carotid artery. 87 75

Collagen, elastin and non-fibrous protein synthesis were measured in the aortas of male New Zealand white rabbits fed a diet containing 2% cholesterol for 140 or 180 days. At these time periods increases in aortic cholesterol and cholesteryl esters were evident. The atherosclerotic lesions induced were predominantly of the foam cell type although some areas of early fibrous lesion formation were noted. These changes in lipid concentration and arterial morphology were accompanied by a significant increase in collagen synthesis as determined by the formation of [14C]hydroxyproline. This increase, however, was not confined specifically to collagen since both elastin and non-collagenous proteins were also being synthesized at a higher rate. The two-fold increase in the rates of both fibrous and non-fibrous protein synthesis may in part be a consequence of marked intimal hyperplasia necessitating a general increase in protein synthesis.
Atherosclerosis 1977 Aug
PMID:Stimulation of aortic protein synthesis in experimental rabbit atherosclerosis. 88 2


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