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)

Human aortic smooth muscle cells were cultured in the presence of sera from 7 normolipidemic women before and after treatment with high-dose medroxyprogesterone acetate, which caused 16% and 25% decreases in serum cholesterol and HDL-cholesterol concentrations, respectively. As assessed by cell counting and by DNA determination the growth of the cells was retarded significantly in the presence of sera taken after the treatment. At the same time, there were no marked changes in the incorporation rate of [3H]proline into collagen or [3H]glucosamine into hyaluronic acid by the cells. The results indicate that: (1) the mitogenicity of human serum can be altered by drug treatment of serum donors, (2) simultaneously with a lowering of serum lipids in man in vivo, a decreased mitogenicity of sera occurs in vitro.
Atherosclerosis 1987 Oct
PMID:Growth of human aortic smooth muscle cells cultured with human serum is retarded when serum lipids are lowered by medroxyprogesterone. 296 Mar 27

Proteoglycan (PG) metabolism by aortic smooth muscle cell cultures derived from atherosclerosis-susceptible White Carneau (WC) and -resistant Show Racer (SR) pigeons was compared using [35S]sodium sulfate and [3H]serine or [3H]glucosamine as labeling precursors. Chondroitin sulfate (CS) PG and dermatan sulfate (DS) PG were the major PG secreted into the medium by both cell types. Total PG production, whether measured by incorporation of radiolabel into either core protein or glycosaminoglycan chains, was consistently lower in WC compared to SR cultures at several time points. This difference was due in part to lower (30-37%) PG synthesis in WC cells, but degradation of newly synthesized PG was an important contributor. A pulse-chase study indicated that of the total radiolabeled PG present at time O, only 47% was present at 24 h in WC cultures compared to 88% in SR cultures. The large CS-PG appeared to be the primary target for degradation in WC cells, and this selective processing resulted in a higher DS-PG:CS-PG ratio in these cultures. Structural studies indicated similar core protein and glycosaminoglycan chain sizes within a PG type for both cell types. PG monomer composition differed, however, by a higher sulfation of WC CS-PG compared to SR CS-PG and by a disaccharide sulfation position favoring 6-sulfation in WC PG and 4-sulfation in SR PG.
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PMID:Distinct synthetic and structural characteristics of proteoglycans produced by cultured artery smooth muscle cells of atherosclerosis-susceptible pigeons. 313 65

To elucidate whether or not a vitamin E-deficient diet affects the rat aorta extracellular matrix, we examined the alterations in glycosaminoglycans (GAGs), as one of the components of the extracellular matrix of the aorta. The total amount of uronic acid, as an index of GAG, decreased significantly in the aorta of vitamin E-deficient rats. The components of GAG were identified as hyaluronic acid (HA), heparan sulfate (HS), dermatan sulfate (DS) and chondroitin sulfate (CS) by electrophoresis together with enzymic digestion. The amount of sulfated GAGs, especially the amount of DS and CS, decreased in the aorta of vitamin E-deficient rats. The biosynthetic activity of GAG was determined by using [3H]glucosamine and [35S]sulfate. The total biosynthetic activity of GAG and the incorporation of [3H]glucosamine into HA, HS, DS and CS decreased markedly in the aorta of vitamin E-deficient rats. The decrease in the production of sulfated GAGs, especially DS, which is involved in the potent antithrombogenic activity, could be related to the lower anticoagulant activity in the aorta of vitamin E-deficient rats.
Atherosclerosis 1985 Apr
PMID:Alterations in glycosaminoglycans of the aorta of vitamin E-deficient rats. 392 63

Glycosaminoglycans (GAG) are believed to be important in the pathogenesis of atherosclerosis. We have previously demonstrated that areas of injured aorta that have been re-endothelialized accumulate increased amounts of lipid and GAG when compared to areas remaining de-endothelialized. We have now examined the net incorporation of labeled precursors into the individual GAG present in both re-endothelialized and de-endothelialized areas of rabbit aorta. Aortic tissue was examined at 2-3 and 10-14 weeks after a denuding injury by incubating tissue minces with [3H]glucosamine and sodium [35S]sulfate for 24 hr. Following incubation, the aortic GAG were isolated and assayed for uronic acid concentration and radioactivity. Results indicate that the total GAG concentration was significantly greater (P less than 0.001) in the re-endothelialized (9.46 +/- 0.29 micrograms/mg lipid-free dry residues (LFDR), mean +/- SE) as compared to de-endothelialized (7.89 +/- 0.43 micrograms/mg LFDR) areas. The concentration in uninjured aorta was 9.01 +/- 0.69. The difference between the injured tissues was attributable to increased concentrations of sulfated GAG. Hyaluronic acid and chondroitin sulfate were the most metabolically active of the GAG in either uninjured or injured aorta, together accounting for over 75% of the 3H label. The 3H specific radioactivities of the four GAG in the short-term, re-endothelialized subgroup were all increased nearly twice that found in uninjured and de-endothelialized tissues. With the exception of heparan sulfate, no significant differences were noted in the 3H specific radioactivities between the re-endothelialized and de-endothelialized areas in the long-term subgroup. These results indicate that, relative to adjacent areas of de-endothelialization, GAG preferentially accumulate in re-endothelialized areas even as early as 2-3 weeks following a denuding injury. Overall, metabolic data suggest that increased synthesis is responsible for this effect, although the net contribution of degradative processes cannot be overlooked since GAG turnover was not specifically examined. Thus, it is possible that regenerated endothelium may modify the GAG metabolism of the arterial wall following arterial injury.
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PMID:Altered glycosaminoglycan metabolism in injured arterial wall. 399 53

Rabbit aortic smooth muscle cells cultivated with certain antisera underwent growth changes and necrosis. These cytotoxic antisera were obtained by immunizing rabbits against rat aorta, human or pig aortic glycoproteins, human serum glycoproteins and E. coli lipopolysaccharide. These different antigens share some biochemical characteristics, and contain four main amino acid residues (Glu, Ala, Asp, Gly) and four sugars (mannose, galactose, glucose, N-acetyl glucosamine). The cytolytic properties of these antisera, however, probably correspond to structural analogies, since although ovalbumin is a glycoprotein, anti-ovalbumin antiserum was not cytotoxic. Antibody cytotoxicity against rabbit arterial smooth muscle cells may depend on the biochemical structure of the antigen used to produce antiserum.
Atherosclerosis
PMID:In vitro immune aggression against rabbit aortic smooth muscle cells. 637 15

This study evaluated the effect of hypoxia on the connective tissue metabolism of rabbit aortic smooth muscle cells (SMCs) in culture. When the oxygen saturation of the incubation medium was lowered from 20% to 2-3%, synthesis of sulphated glycosaminoglycans (GAGs) and hyaluronic acid, as determined from the incorporation of [3H]glucosamine, was stimulated. However, this occurred only after 24 h preincubation of the SMCs in hypoxia. The collagen synthesis of the cells was determined from the incorporation of [3H]proline into protein hydroxyproline and calculated in mass units from the specific intracellular precursor radioactivity. The total protein synthesis was similarly determined from the incorporation of [3H]proline into protein-bound proline. Hypoxia decreased the collagen synthesis, but did not affect the total protein synthesis of the cells. When compared with the control cultures the cell protein of the SMC cultures kept in hypoxia, decreased on the first day in hypoxia whereafter it increased. These results may explain the mechanisms by which hypoxia affects the connective tissue metabolism of the arterial wall in vivo.
Atherosclerosis 1984 Feb
PMID:Effect of hypoxia on the synthesis of glycosaminoglycans and collagen by rabbit aortic smooth muscle cells in culture. 671 71

The biosynthesis of the glycosaminoglycans (GAGs) was investigated in vitro in the aortic tissue of the Cynomolgus monkey incubated with [14C]glucosamine. With the use of a new micromethod, it was possible to quantify the glycosaminoglycans and their radioactive distribution in the aortic tissue and incubation medium. Labeled and nonlabeled chondroitin 6-sulfate, dermatan sulfate, heparan sulfate and hyaluronic acid were measured. Since the sensitivity of this procedure is between 5 and 20 micrograms of GAGs, as little as 5 mg of dry defatted aortic tissue is sufficient for chemical and radioactive analyses.
Atherosclerosis 1982 Dec
PMID:A method to evaluate the biosynthesis of glycosaminoglycans by the aorta of Cynomolgus monkey. 681 78

Rabbit aortic smooth muscle cells (SMCs) were successfully subcultured in 10% hyperlipidemic rabbit serum (HLS) for at least 9 passages. SMCs grown in HLS grew into higher cell densities than SMCs cultured in normolipidemic rabbit serum (NLS) for at least 4-5 passages in NLS and HLS, respectively. However, cells cultured in NLS and HLS for up to 7 passages had similar growth characteristics when they were trypsinised and seeded to grow in 10% fetal calf serum (FCS). Incorporation of [3H]glucosamine into GAGs was taken to represent their rate of synthesis. As compared with cultures incubated in 10% NLS, incubation of rabbit aortic SMCs in the presence of 10% HLS increased the synthesis of sulphated GAGs secreted into the pericellular space by 35% during the first 24 h of contact with HLS. After preincubation for one week in the presence of HLS the synthesis of sulphated GAGs secreted into the incubation medium and into the pericellular space was stimulated by 95% and 34%, respectively. The stimulation of the synthesis of sulphated GAGs by HLS continued for up to 4 weeks at least if the contact of the cells with HLS was maintained. When the cells were subcultured in the presence of NLS and HLS and seeded to grow in FCS after the 1st, 3rd and 7th trypsinisations, the synthesis of sulphated GAGs in cultures of cells from both sources was similar.
Atherosclerosis 1982 Mar
PMID:Long-term effect of hyperlipidemic serum on the synthesis of glycosaminoglycans and on the rate of growth of rabbit aortic smooth muscle cells in culture. 708 20

Glycosaminoglycan (GAG) and lipid synthesis in smooth muscle cells cultured from normal and atherosclerotic rabbit aortas were studied. The incorporation of [14C]glucosamine into acidic GAGs taken to represent their synthesis rate, was enhanced in cells from atherosclerotic aortas as compared with controls. The synthesis of sulphated glycosaminoglycans was affected most and the percentage of radioactivity incorporated into sulphated GAGs was 48 +/- 3% in cells from atherosclerotic and 38 +/- 4% in cells from healthy aortas. Non-radioactive GAGs secreted into incubation media were fractionated by electrophoresis. There was an elevated ratio of sulphated GAGs to hyaluronic acid in the cultures of cells from atherosclerotic aortas and the fraction corresponding to dermatan sulphate was increased most. The incorporation of [3H]oleate into phospholipids was enhanced in cells from atherosclerotic aortas indicating more rapid synthesis of this lipid fraction in these cells. Concentrations of free and esterified cell cholesterol were similar. The results indicate that the enhanced synthesis of sulphated GAGs typical of proliferative atherosclerosis in vivo is maintained in the third passage cultures of cells from atherosclerotic rabbit aortas. In addition there was an enhancement in the synthesis of phospholipids in these cells.
Atherosclerosis 1980 Nov
PMID:Metabolism of glycosaminoglycans and lipids in smooth muscle cells from atherosclerotic rabbit aortas in culture. 745 89

Alteration of glycosaminoglycans (GAGs) in cultured bovine aortic smooth muscle cells after exposure to cadmium was investigated. It was revealed that cadmium increased the accumulation of GAGs metabolically labeled with [3H]glucosamine but decreased that with [35S]sulfate in the cell fraction, the cell surface fraction and the medium fraction. This suggested that cadmium stimulated the biosynthesis of GAGs but inhibited their sulfation in the cells. A similar alteration was observed in cadmium-treated human aortic smooth muscle cell layer. Of tested cations including cadmium, bismuth, cobalt, copper, lead, manganese, nickel and zinc, only cadmium stimulated [3H]glucosamine incorporation, with a strong inhibition of the [35S]sulfate incorporation in the bovine cells. Characterization of bovine smooth muscle GAGs showed that the cadmium-induced increase in the [3H]glucosamine incorporation was mainly observed in heparan sulfate; the inhibition of the [35S]sulfate incorporation occurred non-selectively. Cadmium accumulated in bovine vascular smooth muscle cells in a dose-dependent manner with an increase in the leakage of lactate dehydrogenase into the medium. The present data suggest that vascular smooth muscle cells respond to the cytotoxicity of cadmium and promote the GAG synthesis with a reduction of their sulfation. It is postulated that this response may be a defensive one to the damage of the vascular tissue caused by cadmium but would be a component of the metal-induced atherosclerosis.
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PMID:Alteration of glycosaminoglycans induced by cadmium in cultured vascular smooth muscle cells. 799 22


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