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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of hyperlipidemic, normolipidemic and high-density-lipoproteinemic (HD lipoproteinemic) sera from active runners were studied on cultured human aortic smooth muscle cells. The synthesis of DNA, hyaluronic acid and sulphated glycosaminoglycans (GAGs) in the presence of the various sera was measured by the incorporation of [3H]-thymidine and [3H]-glucosamine. The HD lipoproteinemic sera from runners stimulated the synthesis of DNA and sulphated GAGs less than normolipidemic and hyperlipidemic sera. The hyperlipidemic sera stimulated the synthesis of DNA slightly more than the other sera, but only after a 24 h preincubation. Accordingly, the concentration of HDL-cholesterol in serum was negatively correlated with the synthesis of DNA (r = -0.77, P less than 0.01) and sulphated glycosaminoglycans (r = -0.81, P less than 0.01). The sulphated GAGs/hyaluronate ratio was smaller in the presence of HD lipoproteinemic serum as compared with the other sera. The proliferation of aortic smooth muscle cells and the rate at which they synthesize sulphated GAGs have been considered important during the initiation of atherosclerosis in vivo. The present results suggest that sera having differences in the relative amounts of various lipoprotein fractions differ significantly in their influence on both of these arterial smooth muscle cell functions in vitro.
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PMID:Effect of sera from hyperlipidemic subjects and high-density lipoproteinemic runners on the synthesis of DNA and glycosaminoglycans by cultured human aortic smooth muscle cells. 22 58

1. Carbohydrate composition of serum low and high density lipoproteins obtained from 5 nonhuman primate species (chimpanzee, patas, baboon, rhesus, and spider) and humans was studied. 2. Individual lipoproteins were isolated from pooled sera of each species by ultracentrifugal flotation between the densities 1.019-1.063 for LDL-2; 1.063-1.12 for HDL-2; and 1.12-1.21 for HDL-3. After delipidation, sialic acid, fucose, glucosamine, mannose, galactose, and glucose were determined on apo LDL-2, apo HDL-2, and apo HDL-3. 3. Glucosamine, galactose, and mannose constituted a major component of the sugars in apo LDL-2, with similar relative proportions in all species. Sialic acid, fucose, and glucose formed a minor component, the proportions of which varied greatly among the species. 4. Unlike apo LDL-2, sialic acid, fucose, and glucosamine constituted the bulk of the sugars in apo HDL-2 and apo HDL-3. Mannose, galactose, and glucose were minor components, with galactose predominating. 5. Qualitative differences were observed in electrophoretic mobilities of apo HDL-2 and apo HDL-3 on polyacrylamide gel. One faster moving band was unique to chimpanzee. 6. Intraspecies differences in the content of sialic acid and fucose of apolipoproteins may be related to lipoprotein metabolism and species susceptibility (or resistance) to either spontaneous or diet-induced atherosclerosis.
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PMID:Carbohydrate composition of serum low and high density lipoproteins of nonhuman primate species. 23 83

Three groups of each 12 rabbits were fed a cholesterol-enriched diet. Glucosamine was added in amounts of 0.5% and 2.0% (w/w) to the diet of two of the groups, while the third group served as a control group. The amount of cholesterol in the diet was individually adjusted, so that all rabbits experimental period. Glucosamine did not affect the concentration response of serum cholesterol to dietary cholesterol or the amount of free and esterified cholesterol in the inner aorta. It did, however, cause an increase in the wet weight of the inner aorta with a corresponding decrease in the concentration of aortic cholesterol. Furthermore a decrease in the ratio between mono-unsaturated and di-unsaturated fatty acids of the cholesterol esters of serum and inner aorta were observed in the animals which received glucosamine.
Atherosclerosis 1977 Feb
PMID:Glucosamine and experimental atherosclerosis. Increased wet weight and changed composition of cholesterol fatty acids in aorta of rabbits fed a cholesterol-enriched diet with added glucosamine. 83 56

The effect of hyperlipidemic rat serum and its fractions on the synthetic functions of embryonic fibroblasts was studied. Moderately hypercholesterolemic sera (100-140 mg/100 ml) stimulated the synthesis of collagen, but not the synthesis of non-collagenous proteins nor the incorporation of glucosamine or cytidine. The stimulating principle was nondialyzable. It was not associated with the isolated total lipoproteins but was found in the infranatant fraction of sera centrifuged at a density of 1.220.
Atherosclerosis
PMID:Effect of hyperlipidemic rat serum on the synthesis of collagen by chick embryo fibroblasts. 114 29

Glycosaminoglycans are heteropolysaccharides composed of disaccharide repeating subunits, each one containing a uronic acid component (glucuronic or iduronic acid) and a hexosamine (N-acetyl-glucosamine or N-acetyl-galactosamine, which may be differently sulphated). The presence of GAGs in human plasma has been demonstrated in several studies; they are bound to plasma proteins through non-covalent linkages. However, very little is known about either their origin or their physiological role. Due to their anionic charge, they may influence some metabolic processes, such as blood coagulation, and they could also have a role in urolithiasis and atherogenesis. Moreover, they may be important in modulating the metabolism of some lipoproteins by affecting the rate of their catabolism. Modifications of GAG pattern have been described in a few pathological conditions such as mucopolysaccharidosis, connective tissue diseases and kidney diseases. A high frequency of accelerated atherosclerosis has been observed in haemodialysis patients (HD), probably associated with the altered lipoprotein profile, which is often described in these subjects. Since GAGs may play a role in lipoprotein metabolism, we isolated and characterized plasma GAGs from a group of HD patients and a group of normal matched subjects. Quantitative analysis of plasma GAGs showed a significant increase of these polysaccharides in the HD group. Circulating levels of GAGs were 8.21 +/- 1.89 micrograms/ml in control subjects, and 15.08 +/- 3.13 micrograms/ml in the HD group (p < 0.0001). The isolation of plasma GAGs by ion-exchange chromatography produced two uronic acid containing families: a low-charge (peak I) and a high-charge (peak II) species. Both of these contained GAGs associated with plasma proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Characterization of plasma glycosaminoglycans in hemodialysis patients]. 130 20

We studied the effect of heparin on proteoglycan synthesis by bovine aortic smooth muscle cells in culture. Confluent, growth-arrested cells were incubated with [35S]sulfate, [3H]glucosamine or [3]serine in the presence of 0-600 micrograms/ml heparin. Metabolically labeled proteoglycans secreted into the culture medium and associated with the cell layer were analyzed. In cultures treated with heparin there was a dose-dependent increase in [35S]sulfate incorporation into secreted proteoglycans which reached a maximum (35% above controls) at 100 micrograms/ml heparin. At higher concentrations of heparin, the stimulatory activity declined and finally disappeared. Radioactivity in cell-associated proteoglycans increased significantly (16% above controls) only in cultures treated with 100 micrograms/ml heparin. Heparin also produced similar increases in the incorporation of [3H]glucosamine and [3H]serine into secreted and cell-associated proteoglycans. While chondroitin sulfate, dermatan sulfate and heparan sulfate were elevated in the media, only chondroitin sulfate and heparan sulfate were increased in the cell layer. Heparin did not alter the degradation of proteoglycans. Heparin, while inhibiting the proliferation of subconfluent smooth muscle cells, also stimulated to a greater extent the incorporation of [35S]sulfate into proteoglycans. Other glycosaminoglycans, such as heparan sulfate, dermatan sulfate, heparin hexasaccharide and Sulodexide caused a significant but lesser stimulation of proteoglycan synthesis, while chondroitin sulfates and hyaluronic acid had no effect. Gel filtration chromatography of proteoglycans and their constituent glycosaminoglycans from heparin-treated and untreated cultures showed no differences in their molecular size. The results indicate that heparin can stimulate proteoglycan synthesis by vascular smooth muscle cells irrespective of their state of proliferation. This might have implications in vessel wall repair and arterial wall lipid deposition.
Atherosclerosis 1992 Jun
PMID:Heparin stimulates proteoglycan synthesis by vascular smooth muscle cells while suppressing cellular proliferation. 163 67

Glycosaminoglycans (GAG), which form the elementary constituent of extracellular matrix proteoglycans (PG), are implicated in the pathogenesis of atherosclerosis, mainly due to their lipoprotein binding capability and their abundance in a developing lesion during atherogenesis. However, the reasons for the increment of GAG content are poorly understood. In the present study, the influence of two well known atherogenic factors on arterial GAG synthesis were examined by estimating the incorporation of [14C]glucosamine into aortic GAG in an in vitro incubation system. Radioactivity associated with GAG was taken to represent their synthesis. GAG synthesis by neointimal tissue of rabbit aortas, 12 weeks following balloon catheter deendothelialization was measured and compared in rabbits fed a normal or 0.25% cholesterol supplemented diet for the preceding 6 weeks. In normolipaemic rabbits synthesis was found to be 12,438 +/- 173, 17,884 +/- 1390 and 15,960 +/- 1355 dpm/mg dry defatted tissue from uninjured (control), deendothelialized (DEA) and reendothelialized (REA) areas of rabbit aortas, respectively. This incorporation of radioactivity was significantly greater in hypercholesterolaemic rabbits corresponding to 13,426 +/- 239, 32,670 +/- 3077 and 27,496 +/- 3287 in the control, DEA and REA, respectively. The results demonstrated a synergistic effect of cholesterol feeding and arterial endothelial denudation in stimulating GAG synthesis. Although GAG synthesis was found to be stimulated by either cholesterol feeding or arterial injury, the stimulation by cholesterol feeding alone was only marginal. Further, results show a much higher retention of newly synthesized GAG by the tissue from REA. This study provided a possible explanation for increased GAG content in a developing proliferative lesion.
Atherosclerosis 1992 Jul
PMID:Enhanced incorporation of [14C]glucosamine into glycosaminoglycans of aortic neointima of balloon-injured and cholesterol-fed rabbits in vitro. 164 93

Cell surface proteoglycans of aortic smooth muscle cells of atherosclerosis-susceptible White Carneau (WC) and atherosclerosis-resistant Show Racer (SR) pigeons were compared to determine differences that may be involved in the greater proliferative properties of cultured WC cells. Using [35S]-sodium sulfate and [3H]-glucosamine as labeling precursors, chondroitin sulfate-proteoglycan (CS-PG) and heparin sulfate-proteoglycan (HS-PG) were identified as distinct molecules associated with the plasma membrane. Heparan sulfate-proteoglycan was reduced up to 50% in WC compared with SR cells, and, based on interaction with ion-exchange resin, had a lower charge density. These differences were not observed for the CS-PG from the two cell types. The mode of association of the cell surface PG with the plasma membrane was examined. Dissociation with 1 mol/l (molar) sodium chloride indicated that less than 10% of total cell surface PG were ironically associated with the cells. The remainder required detergent extraction, suggesting hydrophobic interactions with the plasma membrane. Both CS-PG and HS-PG displayed affinity for octyl sepharose and both were identified in isolated plasma membranes. These data present the first description of a hydrophobic CS-PG that is a significant and distinct cell-associated PG in arterial smooth muscle cells. The observation of decreased and structurally altered HS-PG in WC compared with SR cells is consistent with a potential growth regulatory function for this molecule.
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PMID:Cell surface heparan sulfate proteoglycan and chondroitin sulfate proteoglycan of arterial smooth muscle cells. 173 24

To evaluate the effect of hypertension on glycosaminoglycan (GAG) synthesis, cultured vascular smooth muscle cells (CVSMCs) from the aorta of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were exposed to centrifugal forces and catecholamines. GAG synthesis of CVSMCs was measured by the incorporation of [3H]glucosamine into GAGs which were secreted into the culture medium for 24 h. Basal level of GAG synthesis was much higher in SHR than in WKY, when expressed in terms of DNA contents. When exposed to centrifugal force, CVSMCs from rats of both strains synthesized more GAGs. GAG synthesis was enhanced by both noradrenaline (NA) and adrenaline (Ad) in WKY. The enhanced GAG synthesis in WKY by NA or Ad was prevented by pretreatment with propranolol, but not prazosin. In SHR, NA and Ad did not enhance GAG synthesis at this concentration of catecholamines. However, the effects of propranolol or prazosin on GAG synthesis in SHR, when incubated with either NA or Ad, were compatible with the phenomena observed in WKY. Adding dibutyryl cyclic AMP to the culture medium enhanced GAG synthesis in rats of both strains. These data suggest that not only the mechanical stress of high intra-arterial pressure but also beta receptor stimulation, via increasing cyclic AMP, enhance GAG synthesis of vascular smooth muscle cells in hypertension.
Atherosclerosis 1990 Aug
PMID:Effect of centrifugal force and catecholamines on glycosaminoglycans synthesis of vascular smooth muscle cells in culture. 224 93

Because of the importance of glycosaminoglycans and glycoproteins in the pathogenesis of atherosclerosis, the hexosamine concentrations of plasma were determined in 28 male survivors of acute myocardial infarction and in 50 healthy males aged 30-60 years. Glucosamine and galactosamine were determined by ion-exchange chromatography of hydrolyzed whole plasma and hydrolyzed deproteinized plasma. Considerably higher plasma levels of non-protein-bound hexosamine (500 nmol/ml) and lower levels of protein-bound hexosamines (3770 nmol/ml) were observed in the ischemic heart disease group, compared with the plasma levels of non-protein-bound hexosamine (320 nmol/ml) and protein-bound hexosamine (4260 nmol/ml) of the control group. This difference is due to changes in glucosamine concentration. The galactosamine concentration is similar in the two groups. The ratio of non-protein-bound to protein-bound hexosamines in patients is about twice as high as the ratio found in controls. The glucosamine/galactosamine ratio of protein-free plasma is significantly higher in patients (12.1) than in controls (8.3). These changes in plasma hexosamines correlate with increased plasma homocysteine, cholesterol, and triglycerides observed in the patient group. The findings show that characteristic quantitative and qualitative changes in plasma hexosamine levels accompany atherosclerosis. Determination of these substances may be helpful in diagnosis and management of patients with atherosclerosis.
Atherosclerosis 1990 May
PMID:Plasma glucosamine and galactosamine in ischemic heart disease. 236 Sep 22


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