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)

Anti-apolipoprotein A-1 (Apo A-1) autoantibodies were described in autoimmune disorders such as systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) and might be involved in the genesis of arterial and venous thrombotic events. To investigate the presence of these autoantibodies in patients with acute coronary syndrome (ACS) without other features of autoimmunity, we set up an enzyme-linked immunosorbent assay (ELISA) for anti-Apo A-1 antibodies. We used it to investigate their prevalence in ACS as compared to SLE and APS and correlated them to plasma Apo A-1 and serum amyloid A protein (SAA) concentrations. The prevalence of anti-Apo A-1 autoantibodies in the healthy control group was 1% (1/92), but was significantly higher in other groups: 21% (11/53) in ACS group (P=0.001), 13% (12/92) in SLE and/or APS group (P=0.005). Multiple linear regression revealed a significant correlation between plasma Apo A-1 (r=-0.72, P=0.013), plasma SAA concentration (r=0.76, P=0.0066) and anti-Apo A-1 IgG titre in ACS patients. The presence of anti-Apo A-1 autoantibodies in patients with ACS highlights an additional link between autoimmunity, inflammation and atherosclerosis.
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PMID:Presence of autoantibodies to apolipoprotein A-1 in patients with acute coronary syndrome further links autoimmunity to cardiovascular disease. 1557 29

HDL lipoproteins play an essential protective role against development of atherosclerosis 2 they participate in reverse cholesterol transport, act as antioxidants and have antiinflammatory properties. Antioxidant properties of HDL are associated with enzymes such as paraoxonase, LCAT and apolipoproteins apo A-1, apo A-2. HDLs antiinflammatory functions are associated with inhibition of expression of cellular adhesion molecules. Increase of low HDL-cholesterol concentration is now one of the main goals of treatment of lipid disorders for prevention of atherosclerosis and coronary artery disease. In this article we summarised the role of HDL in atherosclerosis development and influence of fish oils and antioxidant vitamins on lipids and lipoproteins fractions.
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PMID:[High density lipoproteins and atherosclerosis]. 1585 Mar 43

Whole-blood viscosity appears to be an independent predictor of stroke, carotid intima-media thickening, and carotid atherosclerosis. The purpose of this study was to examine for relationships between whole-blood viscosity and blood lipids in young healthy subjects over a range of shear rates. Twenty-seven healthy men and women aged 10 to 25 years having a range of low-density lipoprotein (LDL) cholesterol values 88 to 258 mg/dL and body mass index z scores -1.18 to 2.64 SDs were studied. Whole-blood viscosity at shear rates from 1 to 1000 per second was measured using an automated capillary viscometer. Blood lipids were measured using standard techniques. Triglyceride-rich lipoproteins were isolated by ultracentrifugation at density of <1.020 g/mL, and a high ratio of cholesterol to triglyceride was used as an indicator of lipoprotein remnants. Whole-blood viscosity at shear rates of 100 to 1000 per second showed significant negative correlations with apolipoprotein A-1, but not with high-density lipoprotein cholesterol. Whole-blood viscosity at a shear rate of 1000 per second correlated with LDL cholesterol and inversely with LDL size. On stepwise multivariate analysis, apolipoprotein A-1 accounted for 14.7% of the variation in whole-blood viscosity at a shear rate of 150 per second. This study points to the importance of high-density lipoprotein particle number on whole-blood viscosity at physiological shear rates. The physiological significance of the relationships between whole-blood viscosity and LDL cholesterol and LDL particle size at a very high shear rate remains to be determined.
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PMID:The influence of lipoproteins on whole-blood viscosity at multiple shear rates. 1593 11

High density lipoprotein cholesterol (HDL-C) is a primary risk factor for cardiovascular disease. Apolipoprotein A-1 (apoA1) is the major HDL-associated apolipoprotein. The -75G/A single nucleotide polymorphism (SNP) in the apolipoprotein A1 gene (APOA1) promoter has been reported to be associated with HDL-C concentrations as well as HDL-C response to dietary changes in polyunsaturated fat intake. We examined the effect of this APOA1 SNP on exercise-induced changes in HDL subfraction distribution. From a cohort of healthy normolipidemic adults who volunteered for 6 months of supervised aerobic exercise, 75 subjects were genotyped for the -75G/A SNP. Of these, 53 subjects were G homozygotes (G/G) and 22 were A carriers (A/G and A/A). HDL subfractions were measured by nuclear magnetic resonance (NMR) spectroscopy by adding categories HDL-C 1+2 for the small subfraction, and HDL-C 3+4+5 for the large. The change in total HDL-C after exercise was 0.8+/-7.2 mg/dL (+1.7%), and was not statistically significant. HDL subfraction amounts also did not significantly change with exercise training in the total cohort or in G homozygotes or A carriers. The amount of the large HDL subfraction increased in the G homozygotes and decreased in the A carriers (mean+/-S.E.M., 1.8+/-6.6 mg/dL versus -6.1+/-2.3 mg/dL, p<0.0005). In contrast, the amount of the small HDL subfraction decreased in G homozygotes and increased in A carriers (-1.3+/-6.6 mg/dL versus 4.7+/-1.2 mg/dL, p<0.005). These results show that genetic variation at the APOA1 gene promoter is associated with HDL subfraction redistribution resulting from exercise training.
Atherosclerosis 2006 Mar
PMID:Apolipoprotein A1 genotype affects the change in high density lipoprotein cholesterol subfractions with exercise training. 1600 60

It has been estimated that 92% of individuals with type 2 diabetes, without cardiovascular disease (CVD), have a dyslipidaemic profile. Several guidelines on cardiovascular risk now recommend that patients with diabetes should be considered at high risk of CVD and should thus receive lipid-lowering therapy to reduce low-density lipoprotein cholesterol (LDL-C) to below 2.5 mmol/L. Since their introduction in 1987, statins have revolutionized the management of CVD. The most recent statin to be introduced, rosuvastatin, has been shown to be the most effective at lowering LDL-C, as well as consistently raising HDL-C across the 10-40 mg dose range. This has been confirmed by many studies, including the Measuring Effective Reductions in Cholesterol Using Rosuvastatin Therapy (MERCURY I) study in which rosuvastatin 10 mg was shown to be more effective than commonly used doses of other statins, both for LDL-C reduction and achieving treatment target goals. The effectiveness of rosuvastatin has also been studied in type 2 diabetes patients in three studies: the URANUS (Use of Rosuvastatin vs. Atorvastatin iN type 2 diabetes mellitUS), ANDROMEDA (A raNdomized, Double-blind study to compare Rosuvastatin [10 & 20 mg] and atOrvastatin [10 & 20 Mg] in patiEnts with type II DiAbetes) and CORALL (COmpare Rosuvastatin [10-40 mg] with Atorvastatin [20-80 mg] on apo B/apo A-1 ratio in patients with type 2 diabetes meLLitus and dyslipidaemia) studies. URANUS and ANDROMEDA showed rosuvastatin to be more effective than atorvastatin at reducing LDL-C and achieving treatment target goals. CORALL demonstrated rosuvastatin 10, 20 and 40 mg to be more effective at lowering LDL-C than 20, 40 and 80 mg of atorvastatin, respectively. Ongoing studies will evaluate whether these properties of rosuvastatin translate into beneficial effects on atherosclerosis and significant reductions in cardiovascular events.
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PMID:A review of the efficacy of rosuvastatin in patients with type 2 diabetes. 1603 94

Cholesterol is a major component of atherosclerotic plaques. Cholesterol accumulation within the arterial intima and atherosclerotic plaques is determined by the difference of cellular cholesterol synthesis and/or influx from apo B-containing lipoproteins and cholesterol efflux. In humans, apo A-1 Milano infusion has led to rapid regression of atherosclerosis in coronary arteries. We hypothesised that a multifunctional plasma delipidation process (PDP) would lead to rapid regression of experimental atherosclerosis and probably impact on adipose tissue lipids. In hyperlipidemic animals, the plasma concentrations of cholesterol, triglyceride and phospholipid were, respectively, 6-, 157-, and 18-fold higher than control animals, which consequently resulted in atherosclerosis. PDP consisted of delipidation of plasma with a mixture of butanol-diisopropyl ether (DIPE). PDP removed considerably more lipid from the hyperlipidemic animals than in normolipidemic animals. PDP treatment of hyperlipidemic animals markedly reduced intensity of lipid staining materials in the arterial wall and led to dramatic reduction of lipid in the adipose tissue. Five PDP treatments increased apolipoprotein A1 concentrations in all animals. Biochemical and hematological parameters were unaffected during PDP treatment. These results show that five PDP treatments led to marked reduction in avian atherosclerosis and removal of lipid from adipose tissue. PDP is a highly effective method for rapid regression of atherosclerosis.
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PMID:Plasma delipidation process induces rapid regression of atherosclerosis and mobilisation of adipose tissue. 1604 67

Although high-density lipoproteins (HDL) possess many features that contribute to the association between elevated HDL cholesterol and protection from atherosclerosis, these lipoproteins may be modified in certain individuals and/or circumstances to become proinflammatory. The ability of HDL to inhibit or paradoxically to enhance vascular inflammation, lipid oxidation, plaque growth, and thrombosis reflects changes in specific enzyme and protein components. The anti-inflammatory and proinflammatory functional properties of HDL can now be assessed using cell-based and cell-free assays. Acute or chronic systemic inflammation and the metabolic syndrome appear to render HDL proinflammatory. In contrast, statins and experimental agents such as apolipoprotein A-1 mimetics render HDL more anti-inflammatory. Functional characterization of HDL is a promising method for enhanced assessment of cardiovascular risk and effectiveness of risk reduction.
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PMID:High-density lipoprotein function recent advances. 1628 61

The cardiovascular effects of dietary soy on men or adult male experimental animals have received little attention. We determined the effects of long-term (31 mo) consumption of a commercially available soy protein concentrate containing experimentally varied concentrations of isoflavones on the development of atherosclerosis and vascular reactivity in adult male monkeys. The monkeys were fed atherogenic diets that differed only in the source of protein: Control (n = 30), casein and lactalbumin; low-isoflavone soy (n = 30), a mixture of unmodified soy protein isolate and isoflavone-depleted soy protein isolate containing 0.94 mg of isoflavones/g protein; and high-isoflavone soy (n = 31), unmodified soy protein isolate containing 1.88 mg of isoflavone/g protein. Plasma LDL cholesterol was reduced, whereas HDL cholesterol and apolipoprotein A-1 (P < 0.05) were increased in both groups that consumed soy protein. Atherosclerosis (mean plaque size in the coronary arteries) was reduced by approximately 34% (P < 0.05) in both groups fed soy protein. There were no effects of dietary soy on endothelium-dependent or -independent reactivity of coronary arteries. The results indicate that long-term consumption of soy protein containing a modest amount of isoflavones inhibits the early progression of coronary artery atherosclerosis without affecting endothelium-dependent or -independent arterial function.
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PMID:Soy protein containing isoflavones reduces the size of atherosclerotic plaques without affecting coronary artery reactivity in adult male monkeys. 1631 31

The effects of a white wine enriched with polyphenols (PEWW) from Chardonnay grapes and of a sparkling red wine (SRW) from Pinot Noir and Chardonnay grapes were studied for the first time on early atherosclerosis in hamsters. Animals were fed an atherogenic diet for 12 weeks. They received by force-feeding PEWW, SRW, ethanol 12% (ETH), or water as control (mimicking a moderate consumption of approximately 2 red wine glasses per meal for a 70 kg human). Plasma cholesterol concentrations were lower in groups that consumed PEWW and SRW accompanied by an increase in the ratio apo A-1/apo B. Liver-specific activities of superoxide dismutase and catalase were significantly increased by PEWW (38 and 16%, respectively) and by SRW (48 and 15%, respectively). PEWW and ETH significantly increased plasma antioxidant capacity and vitamin A concentrations. Aortic fatty streak area (AFSA) was significantly strongly reduced in the groups receiving PEWW (85%) and SRW (89%) in comparison with the control. AFSA was reduced by ethanol to a lesser extent (58%). These data suggest that tannins from the phenolics-enriched white wine induce a protective effect against early atherosclerosis comparable to that produced by sparkling red wine containing tanins and anthocyanins and dissociated from the antioxidant action of these compounds.
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PMID:Polyphenols-enriched Chardonnay white wine and sparkling Pinot Noir red wine identically prevent early atherosclerosis in hamsters. 1633 38

There is increasing epidemiologic evidence implying a role for chronic infection in atherosclerosis and that microbial TLR agonists may contribute to this disease. Mycoplasma arthritidis is an agent of acute and chronic inflammatory disease in rodents, and has been used extensively as a model for defining the mechanisms involved in arthritis and other inflammatory diseases. We have purified a 28-kDa, apolipoprotein A-1 (apoA-1)-like TLR2-dependent macrophage-activating moiety from a culture of a virulent strain of M. arthritidis. ApoA-1 similarly isolated from uninoculated mycoplasma medium was without bioactivity. The activity of the mycoplasma-derived molecule was resistant to heat and to digestion with proteinase K, but was susceptible to alkaline hydrolysis and H(2)O(2) oxidation. Infrared profiles of normal apoA-1 and that derived from mycoplasma were distinct. Unlike the activity of other mycoplasmal TLR2 agonists such as macrophage-activating lipopeptide-2, activity of the M. arthritidis-derived 28-kDa component was dependent upon CD14, a coreceptor for LPS. Finally, we showed that bioactive lipopeptides prepared from M. arthritidis grown in serum-free medium and also from a 41-kDa known bioactive lipoprotein of M. arthritidis, avidly bound to purified apoA-1 that separated out by SDS-PAGE, induced TNF-alpha and IL-12p40 both in vitro and in vivo. ApoA-1 is a key functional component of the high-density lipoprotein cholesterol complex by scavenging and removing unwanted lipids. Our finding that this molecule can acquire macrophage-activating properties from microbial TLR2-dependent agonists suggests a novel mechanism whereby some microbial agents might reverse the protective role of apoA-1, thus contributing to the genesis of atherosclerosis.
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PMID:A microbial TLR2 agonist imparts macrophage-activating ability to apolipoprotein A-1. 1698 24


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