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

The in vitro effects of prostaglandins E1 and F1alpha on the activity of cholesteryl ester synthetase and cholesteryl ester hydrolase activities of the pigeon aorta were examined. It was found that prostaglandin E1 markedly inhibited the cholesteryl ester hydrolase activity in the supernatant fraction and slightly inhibited the cholesteryl ester synthetase activity. Prostaglandin F1alpha, however, modestly stimulated the cholesteryl ester hydrolase activity both in the microsomal and in the supernatant fraction of the aorta. These observations strongly warrant further studies on the role of prostaglandins in atherogenesis.
Atherosclerosis 1977 May
PMID:Effect of prostaglandins E1 and F1alpha on the activities of cholesteryl ester synthetase and cholesteryl ester hydrolases of pigeon aorta in vitro. 1 25

Cholesterol ester hydrolase activity was determined in preparations of rabbit and guinea pig aorta utilizing micellar and glycerol-dispersed cholesterol oleate substrates. Both substrate preparations demonstrated an acid pH optimum of 4--5 for the soluble and particulate rabbit media cholesterol ester hydrolase, suggesting a lysosomal origin for this activity. Approximately one-fifth of the total recovered activity was particulate. Particulate media preparations from guinea pig aorta also demonstrated cholesterol ester hydrolase activity at acid pH values with a definite optimum at pH 5 for the glycerol-dispersed substrate. However, in contrast to the rabbit media enzyme, activity was also observed at neutral pH with another optimum at pH 7. The supernatant enzyme from guinea pig media exhibited only a single pH optimum of 7. Cholesterol ester hydrolase activity from either rabbit or guinea pig media was not influenced by preincubation with cyclic AMP, ATP and protein kinase. The addition of chloroquine resulted in the inhibition of both the rabbit and guinea pig enzyme. Cholesterol ester hydrolase activity from rabbit and guinea pig media was also inhibited by phenyl methane sulfonyl fluoride; activity measured at pH 7 (guinea pig) was more sensitive to inhibition than activity measured at pH 5 (guinea pig and rabbit).
Atherosclerosis 1978 Sep
PMID:Characterization of cholesterol ester hydrolase activities in rabbit and guinea pig aortas. 3 Apr 61

This study for the first time examines the biosynthesis and effect of prostaglandin E2 (PGE2) in aorta during genetic atherosclerosis. Biosynthesis of PGE2 from [1-14C]arachidonic acid was investigated in the aorta of spontaneously atherosclerosis-susceptible White Carneau pigeons and was compared with that of the atherosclerosis-resistant Show Racer breed. Most of the PGE2 synthetase activity was located in the microsomes. The synthesis was linear up to an hour and was optimal at pH 7.4. The formation of PGE2 in the aorta in the White Carneau pigeons was significantly higher (P less than 0.01) than that in age-matched Show Racer pigeons. In vitro PGE2 strongly inhibited the cholesteryl ester hydrolase activity (51.6% inhibition at 4 X 10(-7) M concentration) in the supernatant fraction of the aorta. On the basis of (1) the increased formation of PGE2 in the aorta of atherosclerosis-susceptible pigeons and (2) its effect on specific enzymes that control cholesteryl ester concentration in aorta, it is hypothesized that PGE2 synthesized at a higher rate in damaged aorta has a significant role in cholesteryl ester accumulation during atherogenesis.
Atherosclerosis 1978 Apr
PMID:Prostaglandin E2 biosynthesis and effect in pigeon aorta. Possible role in atherogenesis. 9 45

This study is the first to report the effect of conjugated equine estrogens on the acitivity of cholesteryl ester synthetase and cholesteryl ester hydrolases in the aorta. In spontaneously atherosclerosis-susceptible White Carneau pigeons, estrogens significantly decreased (P less 0.01) the activity of cholesteryl ester synthetase and increased (P less than 0.01) the cholesteryl ester hydrolase activity in the microsomal fraction of the aorta. There was no effect on the cholesteryl ester hydrolase activity in the supernatant fraction. The inhibition of cholesteryl ester synthesis and the stimulation of cholesteryl ester hydrolase might be responsible for the decreased content of cholesteryl esters noted in pigeon aorta after estrogen treatment.
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PMID:Effect of estrogens on the acitivities of cholesteryl ester synthetase and cholesteryl ester hydrolases in pigeon aorta. 20 Oct 55

Phthalazinol (EG 626), a thromboxane A2 antagonist and cyclic AMP phosphodiesterase inhibitor, has been shown to prevent the atherosclerosis induced in cholesterol fed rabbits. In an attempt to clarify the antiatherosclerotic mechanism, the effects of this compound on the lipolytic enzyme activities (cholesterol esterase and lipoprotein lipase) of rat aorta were examined in vivo. Administration of EG 626 (100-200 mg/kg, per os, daily, 1-2 weeks) affected neither the aortic lysosomal cholesterol esterase nor the acid phosphatase activity, whereas the lipoprotein lipase activity was signficantly decreased by the treatment. These results suggest that with an elevation in HDL-cholesterol, a decrease in lipoprotein lipase activity after ingestion of EG 626 might contribute, at least to some extent, to the prevention of arterial lipid accumulation.
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PMID:Effects of phthalazinol (EG 626) on arterial lipolytic enzyme activities in the rat. 23 31

This study for the first time has simultaneously assayed three cholesteryl ester hydrolase activities located in the various subcellular fractions (lysosomal, microsomal, and soluble) of the aorta and their significance in aortic cholesteryl ester accumulation during genetic and cholesterol-fed atherosclerosis is assessed. When the enzyme activities in the aorta of age-matched atherosclerosis-susceptible White Carneau and atherosclerosis-resistant Show Racer pigeons were compared, a decrease in microsomal cholesteryl ester hydrolase activity was found during the period of cholesteryl ester accumulation. However, under cholesterol-fed conditions (which further increase cholesteryl ester accumulation), an increase in lysosomal cholesteryl ester hydrolase activity and a decrease in soluble cholesteryl ester hydrolase activity was found. These studies have documented differences in response in specific cholesteryl ester hydrosases of the aorta to genetic and cholesterol-fed atherogenesis and warrant further studies to investigate the effect of hormonal and dietary factors on the activities of these enzymes.
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PMID:Significance of various cholesterol, ester hydrolases in aorta. 44 26

Hypertension is an important risk factor for atherosclerosis and often occurs in association with diabetes mellitus. Specific activities of hydrolases in homogenates of aortas from rats with renal-clip hypertension, normotension following a period of hypertension, and hypertension combined with streptozotocin-induced diabetes mellitus were measured. Enzymes included: neutral alpha-glucosidase, and lysosomal N-acetyl-beta-glucosaminidase, beta-galactosidase, cathepsin C, acid alpha-glucosidase, and acid cholesteryl esterase. After 6 or 12 weeks of hypertension, specific activities of all enzymes measured were significantly increased, levels ranging from 24% above normal for cathepsin C to 351% above normal for N-acetyl-beta-glucosaminidase. Six weeks of normotension following 6 weeks of hypertension resulted in restoration to normal of four of the six enzyme activities; the remaining two enzymes were significantly below normal levels. Combined hypertension and diabetes mellitus showed smooth muscle cell levels of four of the five hydrolases measured to be significantly lower than those present with hypertension alone. In every instance, histochemical studies of aortas showed acid phosphatase and N-acetyl-beta-glucosaminidase activities which corresponded to the biochemical findings. These findings indicate profound and discrete effects of two clinical risk factors on vascular smooth muscle cell lysosomes.
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PMID:Hydrolase activities in the rat aorta. II. Effects of hypertension alone and in combination with diabetes mellitus. 65 43

Guinea pigs were fed a semisynthetic diet containing 10% (by weight) cottonseed oil with or without 1% cholesterol. In response to cholesterol/fat feeding there was a significant accumulation of cholesteryl ester (CE), particularly in the liver, but also in the kidney, spleen and suprarenal glands. The hepatic acyl-CoA:cholesterol acyltransferase (ACAT) increased 5-10 times when the animals were fed cholesterol fat during 11 weeks while the acid cholesterol esterase (CE-ase) was similar in the two dietary groups. Intestinal lymph showed the highest content of cholesterol (both free and esterified) in guinea pigs fed cholesterol/fat. A low activity of lecithin:cholesterol acyltransferase (LCAT) was present in the intestinal lymph, irrespective of dietary composition. Triglyceride-rich lipoproteins seem to inhibit LCAT activity in the intestinal lymph. Plasma cholesterol levels in animals fed cholesterol/fat increased markedly while LCAT remained unaffected by the diets. Activity of ACAT and CE-ase in kidney and spleen was low compared to liver tissue and the enzyme activities were not affected by the cholesterol/fat feeding.
Atherosclerosis 1978 Jun
PMID:Cholesteryl ester metabolism in fat- and cholesterol/fat-fed guinea pigs. 67 14

The in vitro activity of cholesteryl ester hydrolase preparations of rat and rabbit aortas was assayed in the presence of the taurine and glycine conjugates of cholic, chenodeoxycholic, deoxycholic and lithocholic acids or in the presence of Triton X-100 and Tween-20. Maximum activity was obtained with tauro- or glycocholic acids. As in the case of pancreatic cholesteryl esterase, trihydroxycholanoic acid derivatives may serve an obligatory function.
Atherosclerosis 1978 Nov
PMID:Aortic cholesteryl esterase. Influence of bile salts. 71 40

Among the many, multifactorial etiologies of atherosclerosis is excessive filtration and deposition of lipids, particularly cholesterol esters, in arterial walls; furthermore, the monoclonal theory purports that the artheroma is an uncontrolled proliferation of cells similar to a benign tumor. These 2 aspects of atherosclerosis pathogenesis were studied in 5 healthy women on birth control pills by investigating the level of mononuclear cell cholesterol ester hydrolase (CEH). Control subjects underwent identical investigation. Mononuclear CEH activity was signficantly lower in women on oral contraceptives than in controls in 4 of the 5 test intervals and showed no signficant fluctuation in activity. Average value of CEH in 5 women on birth control pills was 927+ or -81 pmol/mg of protein/hour. In 5 men followed at 5-day intervals, no significant fluctuation of CEH activity was found. Mean average was 2373+ or -92. Total cholesterol and its ester in both plasma and mononuclear cells showed no signficant differences at the 5-day intervals between men and women. However, plasma cholesterol/cholesterol ester ratios were significantly higher in women than men at each of the 5-day intervals from Days 5-25. An additional link between female hormones and atherosclerosis is suggested by the finding that women on oral contracepitves, known to be predisposed to premature atherosclerosis, show reduced and nonfluctuating levels of mononuclear cell CEH.
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PMID:The effect of oral contraceptives on mononuclear cell cholesterol ester hydrolase activity in premenopausal women taking oral contraceptives: relevance to atherosclerosis. 75 88


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