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)

LDL-apheresis (immunoabsorption, heparin precipitation (HELP), dextran sulfate cellulose binding (DSC) or filtration) is a potent therapeutic tool in familial hypercholesterolemia (FH) to eliminate LDL-cholesterol, Lp(a) or fibrinogen from the circulation and improve blood rheology. Repetitive use can deplete the cholesterol pool between 40 and 80%. As first reports showed, progression of coronary atherosclerosis can be stopped and sometimes regression can be induced. So far the domain of plasmapheresis was homozygous familial hypercholesterolemia. With several apheresis methods now available, it seems timely to define the indication of plasma therapy for heterozygous FH and the place of this potent therapeutic tool in primary and secondary prevention of atherosclerotic coronary heart disease in patients suffering from severe hypercholesterolemia resistant to diet and/or drug therapy.
Atherosclerosis 1991 Jan
PMID:LDL-apheresis: results of longterm treatment and vascular outcome. 206 31

Whereas vascular smooth muscle cell-extracellular matrix interactions have been intensively studied, our knowledge regarding the role that matrix plays in regulating the growth state and contractile phenotype of vessel wall cells is fragmentary. Of particular interest has been the demonstrable ability of (1) heparin to selectively inhibit vascular smooth muscle cell growth in vitro; (2) aortic endothelial cells to produce a heparin-like inhibitor of vascular smooth muscle cells, and (3) heparin to reverse smooth muscle cell proliferation in arteries that have been experimentally denuded of their endothelium. Recent work from our laboratory indicates that the endothelial cell synthesized extracellular matrix alters growth rate and heparin sensitivity of vascular smooth muscle cells. Whereas endothelial cell synthesized matrices that contain collagen and fibronectin promote smooth muscle cell growth, matrices containing heparan sulfate proteoglycan selectively inhibit identical smooth muscle cell populations. Similarly, these heparan sulfate enriched matrices lower smooth muscle sensitivity to heparin and positively influence the endothelial cells' ability to produce the heparin-like inhibitor of vascular smooth muscle cell growth. In an effort to understand the mechanism mediating heparin's effects on smooth muscle cell proliferation and contractile phenotype, we have analyzed the effects of heparin on vascular smooth muscle cell shape and actin isoform expression using doses of heparin previously shown to be growth inhibitory. The results of our studies indicate that heparin alters smooth muscle cell shape and cytoskeletal organization, suggesting that heparin's growth inhibitory action may be related to its effects on cell shape. Additionally, the permissive effects that different endothelial matrices exert on vascular smooth muscle may selectively predispose specific subpopulations of arterial cells towards a proliferating phenotype, one associated with the genesis of atherosclerosis.
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PMID:Endothelial cell matrices modulate smooth muscle cell growth, contractile phenotype and sensitivity to heparin. 208 70

The anti-oxidant action of ferulic acid in gamma-oryzanol was tested in hypercholesterolemic rabbits to determine its effects on the development of atherosclerosis. Eighteen male New Zealand white rabbits were fed a diet containing 1% cholesterol with or without 1% gamma-oryzanol for 10 weeks. The anti-oxidant effect was assessed by the degree of resistance of low density lipoprotein (LDL) to oxidation by copper sulfate and the effect of the copper oxidized LDL on the incorporation of oleate into cholesteryl ester by mouse peritoneal macrophages. In addition, the levels of plasma cholesterol, triglyceride and lipid peroxide were measured before, during and at the end of cholesterol loading. The amount of free ferulic acid and gamma-oryzanol in plasma and LDL and the area of aortic atherosclerotic plaques were determined. It was found that oleate incorporation into cholesteryl ester by macrophages was significantly reduced in the gamma-oryzanol-treated group compared to the non-treated group, and that the reduction was via a mechanism independent of anti-oxidant action. However, no differences were found in the levels of plasma cholesterol, triglyceride, lipid peroxide or in the areas of atherosclerotic plaques between the two groups. It was concluded that gamma-oryzanol has little or no preventive effects on atherosclerosis in rabbits.
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PMID:Effect of gamma-oryzanol on atheroma formation in hypercholesterolemic rabbits. 213 May 37

Serum levels of DHEA sulfate are inversely associated with cardiovascular death in men, and urinary dehydroepiandrosterone (DHEA) levels are inversely associated with clinical manifestations of coronary artery disease. These observations may be related to the antiproliferative effects of DHEA, resulting in inhibition of atherosclerotic intimal hyperplasia. To examine the relation between these steroids and a direct measure of coronary atherosclerosis, plasma DHEA and DHEA sulfate levels were determined in 206 middle-aged patients (103 men, 103 women) undergoing elective coronary angiography. Plasma DHEA sulfate levels were lower in men with at least one stenosis greater than or equal to 50% compared with those without any stenosis greater than or equal to 50% (4.9 +/- 2.7 versus 6.1 +/- 3.5 nmol/ml, p = 0.05). Levels of DHEA sulfate were also inversely related to the number of diseased coronary vessels (r = -0.20, p = 0.05) and a continuous measure of the extent of coronary atherosclerosis (r = -0.25, p = 0.01) in men. The association between DHEA sulfate levels and extent of coronary artery disease was independent of age and other conventional risk factors for coronary disease. In women, there was no association between plasma DHEA or DHEA sulfate levels and coronary disease. These data demonstrate a consistent, independent, inverse, dose-response relation between plasma DHEA sulfate levels and angiographically defined coronary atherosclerosis in men. Plasma DHEA sulfate may be another important and potentially modifiable risk factor for the development and progression of coronary atherosclerosis.
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PMID:Plasma dehydroepiandrosterone and dehydroepiandrosterone sulfate in patients undergoing diagnostic coronary angiography. 214 10

To evaluate the involvement of the complement system in atherogenesis, we investigated the effect of camostat mesilate (CM), C1r, and C1 esterase inhibitor on cholesterol-induced atherosclerosis in rabbits. We also examined the effect of sodium dextran sulfate (DS, molecular weight: 7000), which is reported to be effective in preventing arteriosclerotic diseases and in inhibiting cholesterol-induced atherosclerosis in experimental animals, on complement activation in vitro and in vivo. The administration of CM reduced the formation of atherosclerotic lesions in cholesterol-fed rabbits. DS inhibited complement pathway in vitro, and the administration of DS reduced the C3a level in subjects. These results suggest that complement activation may possibly be involved in the atherosclerotic process.
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PMID:Clinical and experimental approaches to the prevention of atherosclerosis by immunological regulations. 224 58

A 59-year-old woman, one of 5 cases with familial type III hyperlipoproteinemia reported at our clinic to date, had nephrotic syndrome and diabetes mellitus, but had neither coronary atherosclerosis nor xanthoma. A renal biopsy specimen revealed a massive cluster of foam cells containing apolipoprotein B and E in the mesangial region of the kidney. A restricted diet intake combined with lipid-lowering drugs such as cholestyramine, clinofibrate, and bezafibrate, in addition to methylprednisolone was not very effective in lowering serum triglyceride and cholesterol levels within physiological ranges. Therefore, plasmapheresis, using a dextran sulfate-cellulose column, was performed. Repeated plasmapheresis resulted in a marked decrease in both serum total cholesterol and triglyceride. A second renal biopsy specimen performed 2 years later revealed a marked reduction in foam cells with concurrent improvement in her nephrotic syndrome and glucose intolerance. These results suggest that familial type III hyperlipoproteinemia may be responsible for glomerular lipidosis resulting in nephrotic syndrome. They also indicate that plasmapheresis using a dextran sulfate-cellulose column is very effective in the removal of abnormal lipoproteins such as beta-very low density lipoprotein and intermediate density lipoprotein in a case of familial type III hyperlipoproteinemia.
Atherosclerosis 1990 Jan
PMID:Effects of plasmapheresis on familial type III hyperlipoproteinemia associated with glomerular lipidosis, nephrotic syndrome and diabetes mellitus. 231 Apr 24

The long-term patency of the internal mammary artery graft is better than that of the saphenous vein graft in coronary bypass surgery because of a low incidence of atherosclerosis in the internal mammary artery. In search of a possible biochemical explanation of the low degree of atherosclerosis in the internal mammary artery we compared the chemical compositions of human internal mammary artery and saphenous vein obtained from 37 patients undergoing coronary bypass surgery. The levels of esterified cholesterol and free cholesterol were higher in the internal mammary artery than in the saphenous vein (p less than 0.001 and p less than 0.01, respectively), but lower than the levels reported in previous studies for coronary arteries. The amount of collagen was higher in the saphenous vein (p less than 0.001). Heparan sulfate was the major glycosaminoglycan fraction in the internal mammary artery, probably reflecting the higher cellularity and thicker media in the arterial rather than in the venous tissue. The level of dermatan sulfate was higher (p less than 0.001) in the saphenous vein than in the internal mammary artery. This difference is in a direction that could favor atherogenesis in the saphenous vein graft.
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PMID:Biochemical composition of human internal mammary artery and saphenous vein. 231 30

Arterial dermatan sulfate proteoglycan has been shown to increase with atherosclerosis progression, but factors responsible for this increase are unknown. To test the hypothesis that smooth muscle cell proteoglycan synthesis may be modified by macrophage products, pigeon arterial smooth muscle cells were exposed to the media of either cholesteryl ester-loaded pigeon peritoneal macrophages or a macrophage cell line P388D1. Proteoglycans radiolabeled with [35S]sulfate and [3H]serine were isolated from culture media and smooth muscle cells and purified following precipitation with 1-hexadecylpyridinium chloride and chromatography. Increasing concentrations of macrophage-conditioned media were associated with a dose-response increase in [35S]sulfate incorporation into secreted proteoglycans, but there was no change in cell-associated proteoglycans. Incorporation of [3H]serine into total proteoglycan core proteins was not significantly different (5.2 X 10(5) dpm and 5.5 X 10(5) disintegrations per minute (dpm) in control and conditioned media-treated cultures, respectively), but selective effects were observed on individual proteoglycan types. Twofold increases in dermatan sulfate proteoglycan and limited degradation of chondroitin sulfate proteoglycan were apparent based on core proteins separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Immunoinhibition studies indicated that interleukin-1 was involved in the modulation of proteoglycan synthesis by macrophage-conditioned media. These data provide support for the role of macrophages in alteration of the matrix proteoglycans synthesized by smooth muscle cells and provide a mechanism to account for the reported increased dermatan sulfate/chondroitin sulfate ratios in the developing atherosclerotic lesion.
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PMID:Macrophage secretory products selectively stimulate dermatan sulfate proteoglycan production in cultured arterial smooth muscle cells. 231 26

A buffer extract from homogenized human aorta was applied to a Bio-Gel A-15m column, and two cholesterol-containing peaks were resolved. Both fractions of aortic lipoproteins present in the extracts from normal and atherosclerotic intima and stimulated cholesteryl ester (CE) synthesis in J774 mouse macrophages caused unregulated loading with CE. The Vmax of CE formation in the presence of both fractions correlated with the degree of intimal atherosclerosis. An excess of both fractions did not inhibit the uptake of malondialdehyde-treated low density lipoproteins by macrophages; their interaction with the cells was not inhibited either by fucoidin or by dextran sulfate. The uptake of labeled LDL by human fibroblasts was markedly decreased with excess of both fractions. Aortic lipoprotein-mediated CE synthesis (for both fractions) was completely blocked by EDTA in fibroblasts, being decreased by 50% in macrophages.
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PMID:[Stimulation of cholesterol ester synthesis in macrophages by lipoproteins from normal and atherosclerotic human aorta intima]. 239 79

The effect of dietary magnesium (Mg) on the development of atherosclerosis in cholesterol-fed rabbits was investigated. Male New Zealand White rabbits (n = 31) were placed on five kinds of diets: regular, 1% cholesterol, and 1% cholesterol diets supplemented with either 300, 600, or 900 mg (as Mg) of Mg sulfate. The regular and 1% cholesterol diets contained 400 mg of Mg per 100 g. Each rabbit received 100 g daily of the appropriate diet. Additional Mg was well tolerated and did not affect blood pressure or body weight. The rabbits were sacrificed after 10 weeks, and the oil red O-positive atherosclerotic area that covered the aortic intima and the cholesterol content of the aorta was measured. Additional Mg decreased both the area of the aortic lesions and the cholesterol content of the aortas in a dose-dependent manner. The 1% cholesterol diet significantly increased plasma cholesterol and triglyceride concentrations and decreased high density lipoprotein (HDL) cholesterol concentration. Additional Mg had no further effect on cholesterol and HDL cholesterol concentrations, but it slightly decreased the rise in triglyceride concentration. These results indicate that dietary Mg prevents the development of atherosclerosis in cholesterol-fed rabbits by inhibiting lipid accumulation in the aortic wall.
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PMID:Effect of dietary magnesium on development of atherosclerosis in cholesterol-fed rabbits. 240 1


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