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 heart lipoprotein lipase was purified by affinity chromatography on heparin-Sepharose 4B. When crude extracts of heart acetone powder were applied to columsn, about 40% of total lipase activity was bound to the gel and then eluted with 1.5 M NaCl. At this stage the eluted enzyme was purified 1900-fold. Disc gel electrophoresis yielded a single protein band corresponding with lipolytic activity. Minimum molecular weight of the protein was 60,000 as determined by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. The purified enzyme was highly unstable; however, its activity could be partially stabilized at --20C by bovine serum albumin, glycerol, or ethylene glycol. The activity of the purified enzyme (i) had a pH optimum between 7.8 and 8.0; (ii) required serum for full enzymatic activity; apoC-II could be substituted for serum; (iii) was inhibited by by apoC-I in the presence of activated substrate; (iv) was markedly inhibited by NaCl; and (v) was stimulated by heparin.
Atherosclerosis
PMID:Purification and characterization of lipoprotein lipase from human heart. 0 61

Rat heart lipoprotein lipase was highly purified by affinity chromatography using heparin-Sepharose 4B. When extracts of acetone powder were applied to columns, lipase activity was firmly bound to the gel matrix and was later eluted with 1.5 M NaCl. At this stage the eluted enzyme was purified 1500-fold. Disc gel electrophoresis yielded a single protein band corresponding with the enzyme activity. The apparent molecular weight was 60,000. The purified enzyme was highly unstable; however, its activity could be partially stabilized by glycerol or ethylene glycol. In studying the purified enzyme we observed: (i) a cofactor in serum was required for full enzymatic activity; ApoLp-Glu could be substituted for this cofactor; (ii) ApoLp-Ser was inhibitory to lipase activity; (iii) NaCl and protamine sulfate also markedly inhibited the lipase activity; (iv) heparin stimulated the enzymatic activity.
Atherosclerosis
PMID:Rat heart lipoprotein lipase. 120 Nov 47

The sera from most patients with coronary heart disease concurrent with angiographically documented coronary atherosclerosis were found to contain apolipoprotein B (Apo B), neither apolipoprotein E (Apo E) nor apolipoprotein AI (Apo AI) in the circulating immune complexes precipitated by polyethylene glycol-6000 (PEG). Low density lipoproteins are the major components of cholesterol-containing immune complexes precipitated by PEG. A correlation was established between the serum levels of total cholesterol (r = 0,74; p less than 0.01), and low density lipoprotein (LDL) cholesterol (r = 0.77; p less than 0.01) in patients with coronary heart disease and cholesterol in LDL-containing No relationship was found in healthy individuals. The in vitro increase in LDL levels in most patients with coronary heart disease concurrent with coronary atherosclerosis was not followed by an elevation in LDL-containing immune complexes.
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PMID:[Relations between the levels of lipoprotein-containing immune complexes and lipids in the blood of patients with ischemic heart disease]. 204 Dec 89

We performed an in vitro study to assess damage to swine aortic endothelial cells by rabbit beta-VLDL and/or rabbit peritoneal macrophages. Incubation of cultured aortic endothelial cells with beta-VLDL, macrophages, or macrophage lysate induced endothelial cell damage time- and dose-dependently as estimated by [3H]adenine release. Incubation of endothelial cells with both beta-VLDL and macrophages produced a synergistic effect on the increase of [3H]adenine release. Pretreatment of the endothelial cells with some kinds of antioxidants (probucol 50 micrograms/ml, vitamin E 50 microM, superoxide dismutase-polyethylene glycol 0.5 mg/ml, or catalase-polyethylene glycol 0.5-1.0 mg/ml) significantly prevented the endothelial damage by beta-VLDL or macrophage lysate. We conclude that beta-VLDL and/or macrophages could induce endothelial cell damage and that some kinds of antioxidants could prevent it.
Atherosclerosis 1990 Dec
PMID:Aortic endothelial cell damage induced by beta-VLDL and macrophages in vitro. 210 79

Blood serum of most patients with coronary heart disease (CHD) caused a 2-5-fold increase in the total cholesterol content of smooth muscle cells cultured from unaffected human aortic intima, i.e. possessed an atherogenic potential manifested in culture. Removal of immunoglobulins G and M from an atherogenic serum brought about a fall in its atherogenic potential. The serum deficient in immunoglobulins A retained its ability to induce the cholesterol accumulation in cells. Treatment of the CHD patients' serum with 2.5% polyethylene glycol 6000 removed the circulating immune complexes. The serum subjected to this treatment lost its atherogenicity, i.e. failed to increase the cholesterol content in cultured cells. Incubation of smooth muscle cells derived from human aortic intima with circulating immune complexes isolated from an atherogenic patients' serum caused a 1.5-3-fold rise in the intracellular cholesterol. Blood sera of most (89%) CHD patients was characterized by a high cholesterol content in circulating immune complexes. More than 75% of healthy subjects and patients without stenosis of coronary arteries had low level of cholesterol in immune complexes. Blood sera atherogenicity manifested in culture directly correlated with the cholesterol level of circulating immune complexes (r = 0.90). These findings suggest that the atherogenicity of CHD patients blood serum is due to cholesterol-containing immune complexes.
Atherosclerosis 1990 Apr
PMID:Correlation between cholesterol content in circulating immune complexes and atherogenic properties of CHD patients' serum manifested in cell culture. 235 Mar 70

In most patients with coronary heart disease (CHD) and angiographically documented stenosed 1-3 coronary arteries, serum contained cholesterol (C) in the circulating immune complexes (CIC), cholesterol levels in these complexes being directly related to serum atherogenicity, i.e. to their ability to cause a 2-5-fold accumulation of lipids in cultured smooth muscle cells (SMC) of the uninvolved human aortic intima (r = 0.91). Removal of IgG and IgM from the patients' sera led to a 75 and 37% decrease, respectively, in their atherogenic properties displayed in cultured SMC. Much more decrease in the atherogenic potential of the sera was seen in 2.5% polyethylene glycol-induced precipitation of CIC. At the same time, incubation of human aortic intimal SMC with CIC isolated from the atherogenic sera from CHD patients caused a 1.5-3-fold increase in intracellular C levels. It was suggested that CIC cholesterol was a determinant of atherogenicity of the sera from patients with coronary atherosclerosis.
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PMID:[Cholesterol-containing circulating immune complexes--a component of the blood serum in patients with ischemic heart disease that determines its atherogenic properties]. 247 94

The concentrations of cholesterol in the high density lipoprotein (HDL) fraction and the HDL2 and HDL3 subclasses were compared in 333 male renal transplant recipients, 36 male patients on maintenance hemodialysis, and 43 healthy men. The subclasses were separated by a precipitation method using polyethylene glycol 6000 and dextran sulphate. In hemodialyzed patients, total HDL cholesterol and both subclasses were reduced. In renal transplant recipients, both total HDL cholesterol and HDL2 were normal, whereas HDL3 remained reduced, analogous to hemodialyzed patients. It can be concluded that a successful renal transplantation has a beneficial effect on HDL metabolism and thus on the development of atherosclerosis.
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PMID:Changed composition of high-density lipoprotein subclasses HDL2 and HDL3 after renal transplantation. 304 32

Adduction of ethylene glycol moieties to the 3-hydroxy position of cholesterol produces polyoxyethylated cholesterol (POEC), a water-soluble compound that suppresses cholesterol synthesis and esterification in cultured human fibroblasts. Feeding Sprague-Dawley rats a diet containing 2% (wt/wt) POEC with 10 ethoxy groups resulted in a 3-fold increase in hepatic 3-hydroxy-3-methylglutaryl-CoA reductase activity compared to activity in rats pair-fed a diet of standard rat chow. POEC with an average of 20 ethoxy groups (POEC-20) caused comparable changes in hepatic [2-14C]acetate incorporation into non-saponifiable lipids under ad libitum feeding conditions, significantly reduced cholesterol absorption (18% vs 57%), and increased fecal excretion of neutral steroids (5.1 vs 2.0 mg/g food intake). POEC-20 also reduced cholesterol absorption in rats fed a diet enriched with 2% cholesterol (11% vs 31%). Histologic studies of intestinal mucosa and hepatic tissues from rats fed POEC showed no pathologic changes. These experiments indicate that POEC reduces cholesterol absorption and causes compensatory increases in hepatic cholesterol synthesis.
Atherosclerosis 1987 Apr
PMID:The effects of polyoxyethylated cholesterol feeding on hepatic cholesterol synthesis and intestinal cholesterol absorption in rats. 360 8

The cell-mediated immune response against low density lipoproteins (LDL) was demonstrated by the migration inhibition test in patients with various vascular diseases. Anti-high density lipoprotein2 (HDL2) cellular immune response was found only in a few patients. LDL and HDL2 binding factors were detected in about 50% of coronary patients. No significant difference in their occurrence was found between the normolipidemic and hyperlipidemic patients nor between patients with hyperlipidemia type II/b and type IV. On the assumption that lipoproteins may act as auto-antigens by forming immune complexes, the presence of anti-LDL and anti-HDL2 activity was investigated in circulating immune complexes obtained by polyethylene glycol (PEG) precipitation from the sera of coronary patients and controls. Using an ELISA technique, PEG-precipitable anti-LDL activity was detected in 23, 11 and 18% of cases with myocardial infarction, angina pectoris and healthy old subjects, respectively. In the immune complexes obtained from the sera of the healthy young donors no anti-LDL activity was found. Anti-HDL2 activity in the immune complexes was demonstrated only in a few cases from among the patients and elderly persons we investigated.
Atherosclerosis 1983 Oct
PMID:Free and complexed anti-lipoprotein antibodies in vascular diseases. 665 14

Levels of total cholesterol (TC), triglyceride (Tg), high-density-lipoprotein-cholesterol (HDL-C), apolipoproteins A and B (ApoA and ApoB), were assayed in the serum of 63 patients suffering from coronary atherosclerosis, who survived myocardial infarction (M.I.) compared to healthy subjects. TC was assayed by an enzymatic-colorimetric technique: after precipitation with PEG 6000 the same method was used to determine HDL-C. Tg were assessed using total enzymatic method and ApoA and ApoB by RID. On the basis of TC, Tg, HDL-C, ApoA and ApoB values we have identified 6 main patterns, presenting a very characteristic lipaemic model. No significant difference was found between survivors and controls as regards TC and Tg; on the contrary, there was a statistical difference between the two groups for HDL-C, ApoA and ApoB.
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PMID:[Lipid variations in coronary disease]. 712 68


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