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

Cholesterol acyltransferase and cholesterol esterase activities of protein extracts from pig aortas have been examined and the rations of synthesis/hydrolysis rates in the presence of substrates with different fatty acids estimated. The values obtained were in the numerical order: cholesteryl oleate greater than palmitate greater than or equal to linoleate greater than linolenate greater than staerate. The results are discussed in relation to the known different accumulation of cholesterol esters in the arterial wall.
Atherosclerosis
PMID:The arterial acyl-CoA:cholesterol acyltransferase and cholesterol ester hydrolase activities. 119 77

Calcium channel blockers have been shown to retard the development of atherosclerosis in rabbits fed cholesterol-rich diets. The mechanism accounting for this effect is controversial but may be by stimulation of cholesteryl ester hydrolase activity in smooth muscle cells, by amelioration of hypercholesterolemia-induced endothelial dysfunction, or by inhibition of smooth muscle cell proliferation and migration. The effect of calcium channel blockers on the evolution of coronary atherosclerosis in humans has been assessed in two clinical trials. In the Montreal Heart Institute trial, nicardipine did not influence the overall rate of progression and regression; however, nicardipine-treated patients experienced significantly less progression of minimal lesions, defined as stenoses of < or = 20% severity. In the International Nifedipine Trial on Antiatherosclerotic Therapy, nifedipine had no effect on overall progression and regression but reduced the rate of appearance of new coronary lesions. These studies constitute a potentially important new approach to the management of coronary atherosclerosis.
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PMID:Interventions that beneficially influence the evolution of coronary atherosclerosis. The case for calcium channel blockers. 142 44

The change of acid cholesteryl ester hydrolase activity in mononuclear leukocyte following treatment of diabetes mellitus was studied in 21 patients with non-insulin-dependent diabetes mellitus (NIDDM). Enzyme activity before treatment in the patients was significantly lower than that in 14 age-matched healthy subjects (1.20 +/- 0.15; mean +/- S.E. vs. 2.20 +/- 0.17 nmol/mg protein/h, P less than 0.01). Enzyme activity before treatment in the patients was significantly increased (P less than 0.05) after 4-8 weeks of treatment. However, enzyme activity of 1.43 +/- 0.14 nmol/mg protein/h observed after treatment in the patients was significantly lower (P less than 0.01) than that in the healthy subjects. There was a significant negative correlation between enzyme activity before treatment and the increase in enzyme activity following treatment (rs = -0.555, P less than 0.01, n = 21). These results indicate that low level of enzyme activity may be insufficiently improved by the treatment of diabetes, and the risk for the development of atherosclerosis as viewed from the enzyme activity may persist even after the treatment in NIDDM.
Atherosclerosis 1992 Feb
PMID:Acid cholesteryl ester hydrolase activity of mononuclear leukocytes in patients with non-insulin-dependent diabetes mellitus: studies before and after treatment of diabetes. 163 50

Decreased acid cholesterol esterase has been linked to cholesteryl ester accumulation and may be fundamental in the development of atherosclerosis. The present study compared cholesterol esterase activity with the accumulation of cholesterol and its esters in aorta, renal artery and renal preglomerular microvessels. Tissue was obtained from white New Zealand rabbits fed either a control or 2%-cholesterol diet for 1 month. Cholesterol esterase was increased in microvessels from cholesterol-fed animals when compared to aorta and renal artery. Cholesterol feeding generally produced an increase in cholesterol and cholesteryl ester accumulation in all vascular tissues. The percent distribution of esterified/total cholesterol in renal microvessels was decreased consistent with the concomitant increase in cholesterol esterase. In contrast, aorta and renal artery exhibited an increase in cholesterol and cholesteryl ester accumulation and an increase in the percent of esterified cholesterol consistent with a decrease in acid cholesterol esterase after cholesterol feeding. The data suggest that renal microvessels, when compared to aorta and renal artery, may be relatively protected from developing atherosclerotic microvascular lesions through an organ-specific increase in acid cholesterol esterase activity.
Atherosclerosis 1992 May
PMID:Comparative studies on acid cholesterol esterase in renal blood vessels and aorta of control and hypercholesterolemic rabbits. 163 56

Changes in low density lipoprotein (LDL) lipid composition were shown to alter its interaction with the LDL receptor, thus affecting its cellular uptake. Upon incubation of LDL with 5 units/ml cholesterol esterase (CEase) for 1 h at 37 degrees C, there was a 33% reduction in lipoprotein cholesteryl ester content, paralleled by an increment in its unesterified cholesterol. CEase-LDL, in comparison to native LDL, was smaller in size, possessed fewer free lysine amino groups (by 14%), and demonstrated reduced binding to heparin (by 83%) and reduced immunoreactivity against monoclonal antibodies directed toward epitopes along the LDL apoB-100. Incubation of CEase-LDL with the J-774 macrophage-like cell line resulted in about a 30% reduction in lipoprotein binding and degradation in comparison to native LDL, and this was associated with a 20% reduction in macrophage cholesterol mass. Similarly, CEase-LDL degradation by mouse peritoneal macrophages, human monocyte-derived macrophages, and human skin fibroblasts was reduced by 20-44% in comparison to native LDL. CEase-LDL uptake by macrophages was mediated via the LDL receptor and not the scavenger receptor. CEase activity toward LDL was demonstrated in plasma and in cells of the arterial wall such as macrophages and endothelial cells. Thus, CEase modification of LDL may take place in vivo, and this phenomenon may have a role in atherosclerosis.
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PMID:Reduced uptake of cholesterol esterase-modified low density lipoprotein by macrophages. 171 Oct 36

Cholesterol accumulation in macrophages that have migrated in the subintimal space leads to foam cell formation, which is believed to be one of the initiating events in atherosclerosis. In this study we investigated the effect of cholesterol feeding on peritoneal monocyte/macrophage cholesterol content and peritoneal cavity lipoprotein composition in rats. A cholesterol (2%) and cholic acid (1%) diet caused significant hypercholesterolemia in plasma, and at the same time the cholesterol content of peritoneal monocytes/macrophages was increased. At day 7, the cellular cholesteryl ester content had risen to 30.1 micrograms/mg cellular protein from a baseline value of 9.2 micrograms/mg. The unesterified cholesterol content also increased by 56%. At this time, acyl-coenzyme A:cholesterol acyltransferase (ACAT) activity was doubled, whereas neutral and acidic cholesteryl ester hydrolase activities were unchanged. Reversal to the regular chow diet after 7 days of the cholesterol-enriched diet normalized plasma cholesterol levels as well as peritoneal monocyte/macrophage cholesteryl ester content. ACAT activity also decreased toward normal levels. Analysis of the d less than 1.21 g/ml peritoneal lipoproteins isolated by ultracentrifugation revealed the presence, in both normal and hypercholesterolemic rats, of apolipoprotein A-I-rich lipid complexes with pre-beta mobility on agarose gel electrophoresis. The size of the peritoneal lipoproteins was smaller than that of plasmatic high density lipoproteins, and their chemical composition was also different from that of the major plasma lipoproteins. The cholesteryl ester content of peritoneal lipoproteins increased after feeding of the cholesterol-enriched diet. In conclusion, our results show that cholesterol feeding leads to rapid accumulation of cholesteryl esters in monocytes/macrophages. As soon as plasma cholesterol levels are returned to normal, cellular cholesterol content is also normalized.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peritoneal macrophage cholesteryl ester content as a function of plasma cholesterol in rats. 206 32

Acid cholesteryl ester hydrolase activity of mononuclear leukocytes was measured in 52 Type 2 (non-insulin-dependent) diabetic patients. Enzyme activity was significantly lower in the diabetic patients than in 14 age-matched control subjects (0.89 +/- 0.08 (mean +/- S.E.) vs. 2.20 +/- 0.17 nmol/mg protein/hr, p less than 0.01). In diabetic patients undergoing diet treatment only, the enzyme activity was significantly lower in poorly controlled patients than in well controlled patients (0.43 +/- 0.03 vs. 1.15 +/- 0.24 nmol/mg protein/hr, p less than 0.01). In the diabetic patients, there was a significant negative correlation between the enzyme activity and serum total cholesterol or low density lipoprotein cholesterol level (r = -0.361, p less than 0.01, n = 52 or r = -0.630, p less than 0.01, n = 28). These results suggest that a low level of acid cholesteryl ester hydrolase activity in mononuclear leukocyte might play an important role in the progression of atherosclerosis in Type 2 diabetes.
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PMID:Acid cholesteryl ester hydrolase activity of mononuclear leukocyte in type 2 (non-insulin-dependent) diabetic patients. 238 65

The effects of 5 micrograms/ml of 25-hydroxycholesterol; cholestane-3 beta,5 alpha,6 beta-triol; and cholesterol on acyl CoA cholesterol acyltransferase, acid cholesteryl ester hydrolase and neutral cholesteryl ester hydrolase was studied in cultured rabbit aortic smooth muscle cells. After 1 hour incubation, 25-hydroxycholesterol resulted in a fourfold stimulation of acyl CoA cholesterol acyltransferase activity. No stimulation by 25-hydroxycholesterol was noted before 15 minutes or after 5 hours of incubation. Neither cholestane-3 beta,5 alpha,6 beta-triol nor cholesterol influenced acyl CoA cholesterol acyltransferase activity at any time interval. No significant effects of any of the sterols were noted on acid cholesteryl ester hydrolase or neutral cholesteryl ester hydrolase activity. The imbalance between acyl CoA cholesterol acyl transferase and hydrolase activities induced by 25-hydroxycholesterol could result in cholesteryl ester accumulation by arterial smooth muscle cells, which may be associated with atherosclerosis.
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PMID:Effects of cholesterol oxidation derivatives on cholesterol esterifying and cholesteryl ester hydrolytic enzyme activity of cultured rabbit aortic smooth muscle cells. 276 54

Normal arterial foci which take up Evans blue dye (EBD) in vivo are believed to represent atherosclerosis-prone, hemodynamically stressed foci compared to areas which exclude dye. We have used the rabbit EBD model to examine focal aortic hydrolases of blue areas versus white areas, and we report herein significant focal variations of hydrolase activities. Enzymes measured included neutral alpha-glucosidase, N-acetyl-beta-glucosaminidase, alpha-mannosidase, acid alpha-glucosidase, beta-galactosidase, beta-glucuronidase, cathepsin C, and acid cholesteryl esterase (ACE); specific activities were expressed on the basis of tissue DNA. In correlative areas of EBD uptake in normal rabbit aortic arch, ACE activity averaged 17% higher and cathepsin C activity averaged 37% lower than activities of areas free of EBD in the descending thoracic aorta (P less than 0.02). None of the glycosidases studied differed significantly between blue and white aortic areas. These findings indicate that discrete, intrinsic differences of hydrolytic enzyme activities exist in the normal rabbit aorta in areas delineated by in vivo EBD uptake, areas recognized as lesion-prone vs lesion-resistant.
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PMID:Intrinsic focal variations of rabbit aortic hydrolase activities. 276 19

To understand better the mechanism of higher absorption of cholesterol and campesterol in high-responding than in low-responding rhesus monkeys, we measured the concentrations of the two sterols in the micellar fraction isolated from small intestinal content, and also determined their rates of esterification by cholesterol esterase prepared from the small intestinal mucosa. The results show that the concentrations of both cholesterol and campesterol in the micellar fraction were significantly higher in the high- than in low- and intermediate-responding rhesus monkeys. Also the rates of esterification of both sterols are higher in the proximal segment of the small intestine in high-responders than the other two groups. We conclude that the two necessary steps in the process of sterol absorption, namely, the amounts of sterols solubilized in micelles and their esterification within mucosal cells which are higher in high- than in low-responders are responsible for the higher absorption of the sterols in the high-responding rhesus monkeys.
Atherosclerosis 1988 Aug
PMID:Studies on the mechanism of high intestinal absorption of cholesterol and campesterol in high-responding rhesus monkeys. 321 63


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