Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In severe cystic acne we found low levels of high density lipoprotein-cholesterol (HDL-C) and apolipoprotein A (Apo-A) in the presence of normal total lipids. In a larger number of patients, we always observed significantly lower levels of HDL-C and Apo-A than in either age-matched controls or subjects with acne vulgaris. Since lipoprotein lipase is one major determinant of HDL concentration, we assayed the lipase activity in liver and extra-hepatic tissues by the method of Krauss et al. There was highly significant less total and hepatic lipase activity than in age-matched controls. HDL distribution was examined by zonal ultracentrifugation and a decrease in the HDL2 subclass was discovered. Since HDL are inversely correlated to atherosclerosis, cystic acne is one risk factor for atherosclerosis. The linkage between low HDL levels and severe cystic acne should be further investigated.
 ...
PMID:Lipoprotein metabolism and lipoprotein lipase in severe cystic acne. 293 79

The independent roles of human lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) in determining the distribution of apolipoprotein E (apo E) among the plasma lipoproteins has been studied in vitro. In one series of three studies, postheparin plasma (10%) was incubated for 2 h with autologous plasma and the changes in the lipoprotein association of apo E after lipase exposure were determined after lipoprotein fractionation on 4% agarose columns. Specificity for LPL or HTGL was achieved by inhibition with goat anti-human HTGL or with 1 M NaCl, respectively. In another study, LPL and HTGL were partially purified from human postheparin plasma. The independent effects of these enzymes on the lipoprotein association of apo E were then examined after incubation of plasma in the absence or presence of one or both lipases. Data from both types of in vitro study showed that LPL-mediated triglyceride hydrolysis in the absence of HTGL activity was accompanied by a loss of apo E from triglyceride-rich lipoproteins, a gain or no change in the apo E-containing lipoproteins the size of intermediate density lipoproteins (IDL) and inconsistent changes in the apo E mass associated with high density lipoproteins (HDL). HTGL activity, on the other hand, in the absence of LPL, resulted in a redistribution of apo E from lipoproteins the size of IDL and a gain by those of HDL size. These studies thus support previous in vivo studies which pointed toward a specific role for HTGL in the processing of apo E containing IDL.
Atherosclerosis 1988 Sep
PMID:Effect of lipoprotein lipase and hepatic triglyceride lipase activity on the distribution of apolipoprotein E among the plasma lipoproteins. 317 31

To characterize the lipoprotein metabolism of lipid-filled cells of atherosclerotic lesions, uptake of 3,3'-dioctadecylindocarbocyanine (DiI)-labelled low density lipoprotein (LDL), acetylated LDL (Ac-LDL) and beta-very low density lipoprotein (beta-VLDL) was studied by fluorescence microscopy and flow cytometry in primary cultures of enzymatically dispersed aortic cells from cholesterol-fed rabbits. Most of the foam cells were identified as macrophages on the basis of Fc-receptors and high activities of nonspecific esterase and acid lipase, although cholesteryl ester (CE) inclusions were found by filipin staining also in smooth muscle cells (SMCs). During the culture only SMCs proliferated and were confluent in about 1 week. After incubation with DiI-Ac-LDL most macrophage foam cells were brightly fluorescent, but also many SMCs accumulated fluorescence. In SMCs, an excess of LDL inhibited the uptake of DiI-beta-VLDL and DiI-LDL, indicating that these lipoproteins were taken up by the apoB,E receptor; the activity of this receptor was low 2 days after cell isolation but increased considerably during SMC proliferation. DiI-beta-VLDL was not taken up by the macrophage foam cells until after 7 days' culture, when their CE content had decreased, reflecting a feed-back regulation of these receptors as well. Our results indicate that, in primary cultures of enzyme-dispersed cells from rabbit atherosclerotic lesions, most of the foam cells have lipoprotein receptors resembling those described in macrophages and that also many SMCs accumulate Ac-LDL.
Atherosclerosis 1988 Feb
PMID:Lipoprotein uptake in primary cell cultures of rabbit atherosclerotic lesions. A fluorescence microscopic and flow cytometric study. 334 44

In order to assess the possible utility of lectin binding to identify the cellular components of fixed arterial lesions we studied lectin binding in experimental rabbit and monkey vessels, as well as in human atherosclerotic arteries obtained at surgery. The avidin-biotin-peroxidase technique was used to localize the binding of the following biotinylated lectins: Concanavalin A (Con A), Dolicho biflorus agglutinin (DBA), soybean agglutinin (SBA), peanut agglutinin (PNA), Phaseolus vulgaris agglutinin (PHA), Ricinus communis agglutinin (RCA), wheat germ agglutinin (WGA), and Ulex europaeus agglutinin (UEA). PHA demonstrated specific cytoplasmic staining of macrophages in rabbit, monkey, and human tissues and differentiated macrophages from other cell types in atherosclerotic lesions. When morphometric comparisons were made between lesion PHA staining and another macrophage marker, acid lipase, very similar results were obtained. Con A, RCA, and WGA stained macrophages intensely and differentiated them from other cell types in normal reticuloendothelial tissues and lesions, but also stained smooth muscle cells and endothelial cells when these cells developed lipid vacuoles. UEA stained the endothelium of vasa vasorum consistently in human arteries, but staining of artery lumen endothelium was variable. Endothelial cells of rabbit or monkey vessels did not stain with UEA. DBA, PNA, and SBA did not consistently stain any cellular structures in arteries. PHA was found to be an excellent marker to differentiate and quantify macrophages in glutaraldehyde or formalin-fixed, paraffin-embedded experimental and human atherosclerotic lesions. Con A, RCA and WGA merit further detailed study in conjunction with other histochemical tests as possible markers of functional changes in arterial cells during lesion development.
Atherosclerosis 1986 Sep
PMID:Lectin binding to distinguish cell types in fixed atherosclerotic arteries. 353 93

The effect of feeding fish oil (Menhaden) on the progression of rhesus monkey atherosclerosis was determined by feeding diets containing 2% cholesterol and either 25% coconut oil (Group I), 25% fish oil/coconut oil (1:1) (Group II), or 25% fish oil/coconut oil (3:1) (Group III) for 12 months (n = 8/group). The average serum cholesterol levels were 875 mg/dl for Group I, 463 mg/dl for Group II, and 405 mg/dl for Group III. HDL cholesterol levels were 49 mg/dl for Group I, 29 mg/dl for Group II, and 20 mg/dl for Group III. An average of 79% of the aortic intima was involved with atherosclerosis in Group I, 48% in Group II, and 36% in Group III. The aortas of both fish-oil groups (II or III) contained significantly less cholesterol (total, free, and esterified), as well as less acid lipase, cholesteryl esterase, and ACAT activities when compared to the coconut-oil group (I) (p less than 0.05). Microscopically, the aortic and carotid artery lesions were smaller in cross-sectional area and in thickness, and contained less macrophages in the fish-oil groups (II and III) when compared to the coconut-oil group (I) (p less than 0.05). This protective effect was not consistently enhanced by increasing the proportion of fish oil to 3:1 (Group III) over 1:1 (Group II). The results indicate that fish oil-containing diets reduce serum cholesterol levels and inhibit atherosclerosis even in the face of lowered HDL cholesterol levels when compared to a pure coconut oil/cholesterol diet in rhesus monkeys. Therefore, fish-oil diets exert effective protective control of progression of atherosclerosis during severe atherogenic stimuli.
 ...
PMID:Fish oil inhibits development of atherosclerosis in rhesus monkeys. 367 3

Lysosomal acid lipase activity was measured in mononuclear leukocytes of patients selected on the basis of premature cardiovascular disease, with or without hyperlipidemia. Enzyme activity was significantly lower in the patient population (4.8 +/- 1.3 nmol/min/mg protein, n = 190 males) than in an age-matched control population (5.4 +/- 1.3 nmol/min/mg protein, n = 124 males). There was no effect of hypercholesterolemia or hypertriglyceridemia on the enzyme activity. In the group of patients with normal plasma lipids (n = 77), 18% had mononuclear leukocyte acid lipase activity which fell below the control population 5th percentile, and in the range of enzyme activity observed in cells from obligate heterozygotes for inherited acid lipase deficiency (Wolman disease and cholesteryl ester storage disease). Studies of acid lipase activity in families of our patients provided evidence that an autosomal mutation is associated with (or responsible for) this reduced enzymatic activity and may represent an independent risk factor for the premature development of atherosclerosis.
Atherosclerosis 1986 Oct
PMID:Genetic variation of human mononuclear leukocyte lysosomal acid lipase activity. Relationship to atherosclerosis. 377 71

We have studied mechanical factors that could determine how stenosis protects against distal atherosclerosis in cynomolgus monkeys fed an atherogenic diet. Critical aortic stenosis was produced by coarctation of the thoracic aorta. After 3 months, coarcted monkeys had a mean aortic pressure gradient of 25 +/- 1 mm Hg and a 76% +/- 2% lumen stenosis. Aortic wall motion was measured by means of in vivo ultrasonic sonomicrometry. Dynamic tracings of aortic pressure and diameter were recorded simultaneously at standard locations proximal and distal to the stenosis and at comparable sites in noncoarcted control animals. In the proximal aorta, mean blood pressure and pulse pressure were increased (p less than 0.05), but wall motion and intimal lesion area were not different from those determined in control monkeys. In the aorta distal to the coarct, mean blood pressure was no different from that in control animals but pulse pressure was diminished; in addition, there was marked reduction of arterial wall motion (p less than 0.001). This was accompanied by a significant reduction of intimal plaque area (p less than 0.05) and acid lipase activity (p less than 0.001). Thus, inhibition of plaque formation in the distal aorta coincided with reduction of pulse pressure and aortic wall motion rather than with blood pressure or hypercholesterolemia. Inhibition of arterial wall motion may account for the sparing effect often encountered in human arteries distal to stenosing atherosclerotic plaques.
 ...
PMID:Protection from atherosclerotic lesion formation by reduction of artery wall motion. 379 93

Oligosaccharide fragments of heparin were prepared using flavobacterial heparinase. Following sizing, these oligosaccharide fractions were administered (i.v.) to rabbits and were examined for their ability to release lipoprotein lipase. The decasaccharides (dp = 10, Mr avg = 2,800) were the smallest oligosaccharides which resulted in substantial lipase release. The plasma lipase levels obtained with decasaccharides were comparable to low molecular weight heparin and one-third those obtained when heparin was administered at an equivalent dose. The peak plasma lipase concentration was observed 10 min following heparinization and fell off rapidly over the 60-min time course. The lipase release activity paralleled the in vivo pharmacokinetics of the heparin and decasaccharide sample as determined by monitoring their anti-Factor Xa activity. No activation of purified bovine milk lipoprotein lipase or plasma lipase was detectable at the concentrations studied, indicating that the increase in circulating lipolytic activity was due entirely to release. Lipoprotein lipase accounted for a major portion of the released activity with hepatic triglyceride lipase representing the remainder of the lipolytic activity. The sized decasaccharide sample was characterized with regards to its structure and anticoagulant activity. The decasaccharides exhibited reduced anticoagulant activity possibly making it a better drug candidate in the treatment of atherosclerosis.
Atherosclerosis 1986 Nov
PMID:Effect of very low molecular weight heparin-derived oligosaccharides on lipoprotein lipase release in rabbits. 380 Oct 83

Regular intake of alcohol is associated with elevated levels of high density lipoproteins (HDL). Opinions differ, however, on the HDL subfraction which is preferentially influenced by alcohol. In the present study we measured the HDL subfraction lipid and protein concentrations and postheparin plasma lipase activities in chronic alcohol users immediately after cessation of drinking and sequentially during one week of total abstention. The HDL2 mass concentration decreased significantly already during two abstinent days the decline continuing until the 8th day. At this time the mean HDL2 concentration had decreased by 38% from the initial value (P less than 0.05). The HDL2 cholesterol, phospholipid and protein concentrations decreased in approximately similar proportions, whereas the HDL2 triglyceride increased by 40%. The HDL3 mass concentration decreased by 13% but this change was not significant. Also in HDL3 the cholesterol, phospholipid and protein contents decreased to a similar extent but the triglyceride content rose. The postheparin plasma lipoprotein lipase activity decreased by 41% and the hepatic lipase by 37% during the abstention. It is concluded that in chronic alcoholics HDL2 accounts for the major part of the increase in HDL.
Atherosclerosis 1986 Feb
PMID:Rapid decrease in high density lipoprotein subfractions and postheparin plasma lipase activities after cessation of chronic alcohol intake. 396 41

Purified acid lipase was previously shown to hydrolyze the artificial substrate, alpha-naphthyl palmitate, as well as triglycerides and cholesteryl esters and to form cholesteryl esters. To determine to what extent these activities are associated with acid lipase-containing cells in atherosclerotic plaques, we examined rabbit aortas at different stages of experimental lesion induction and human atherosclerotic arteries. Assays of cholesteryl ester formation, and alpha-naphthyl palmitate and cholesteryl ester hydrolysis were performed on homogenates of lesions and the hydrolysis of the artificial fatty acid ester was used as a histochemical marker to identify acid lipase positive foam cells in sections of the same lesions. The volume of lesions occupied by cells stained for acid lipase correlated strongly with the enzyme activities of the arterial homogenates. These results suggest that acid lipase-containing cells may mediate the accumulation of cholesteryl ester during atherogenesis. Since acid lipase activity marks macrophages, these methods may be useful for relating macrophage distribution and function to lesion progression, regression, and complication.
Atherosclerosis 1985 May
PMID:Role of acid lipase in cholesteryl ester accumulation during atherogenesis. Correlation of enzyme activity with acid lipase-containing macrophages in rabbit and human lesions. 400 91


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>