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

The collagen types extracted from intermediate and small sized human arteries were investigated by SDS-polyacrylamide gel electrophoresis (SDS-PAGE) after differential salt fractionation. Limited and repeated pepsin digestion was used to prepare collagen species. Type V, IV and VI collagens were extracted greater in the former relative to in the latter, whereas type I and III collagen were extracted until the last extract. Type I collagen comprised as the major collagen in the intima of various arteries as well as in venous tissue. Type III and V collagens were found to be less in small arteries than in the initial stage of atherosclerosis. Type VI collagen in the intermediate and small arteries was detected on SDS-PAGE.
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PMID:Collagen species in various sized human arteries and their changes with intimal proliferation. 210 67

Ordinarily, HDL1, a fraction of HDL enriched in apoE, is a minor fraction of plasma, but in human subjects and experimental animals eating diets high in fat and cholesterol and in patients with homozygous familial hypercholesterolemia (HFH) or CETP deficiency, HDL1 (or HDLc) concentrations in plasma are increased. However, little is known about the structures, compositions and metabolic sources of HDL1 in HFH patients. To obtain HDL1 for the study, we surveyed several fractions in the HDL density range for apoE by SDS-PAGE. The ratio of apoE to apoAI in the HDL (d = 1.063-1.21 g/ml) of 8 HFH patients was 0.14 +/- 0.03 compared to 0.03 +/- 0.005 in a control group of 8 normolipidemic subjects (P less than 0.001) suggesting that an apoE-rich fraction indeed was present in increased amounts. ApoE/apoAI ratios of lipoproteins of the density range 1.050-1.090 were even higher at 1.5 and 2.0 in 2 patients compared to 0.4 +/- 0.1 in controls, indicating that this density fraction may be particularly enriched with apoE-rich lipoproteins. By contrast, d = 1.020-1.050 g/ml and d greater than 1.090 fractions contained very little apoE. Therefore, we further characterized the d = 1.050-1.090 g/ml lipoproteins of HFH patients and controls. Fractionation of an d = 1.050-1.090 fraction by concanavalin-A chromatography (CONA) yielded an unbound apoE-rich fraction that contained apoE, apoAI and apoC but no apoB, and a bound LDL-like fraction that contained mostly apoB-100, as determined by SDS-PAGE and by solid phase immunoassays, containing monoclonal antibodies directed against apoB, apoE and apoAI. The apoE/apoAI ratio of the CONA unbound fraction of HFH patients was greater, and the fraction also contained more free cholesterol and phospholipids than the fraction of control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1990 Oct
PMID:Apolipoprotein E-rich HDL in patients with homozygous familial hypercholesterolemia. 212 36

Authors determined the plasma levels of total cholesterol, HDL-cholesterol, apoprotein B-100 (apo B-100), apoprotein A-I (apo A-I) and lipoprotein(a) in 202 (139 female and 63 male) randomized blood donors. The phenotypes of lipoprotein(a) were detected by SDS-polyacrylamide gelelectrophoresis and Western blotting. The average plasma total cholesterol concentration of this Hungarian population was 5.7 +/- 1.1 mmol/l. The other lipoprotein parameters were HDL-cholesterol: 1.36 +/- 0.04 mmol/l; and the apoprotein B-100 concentration: 70 +/- 17.4 mg/dl. In these parameters no difference between males and females could be found. The average plasma apoprotein A-I in females was 156.3 +/- 23.6 mg/dl and in males 143.8 +/- 26.8 mg/dl and the difference was statistically significant (p less than 0.01). The average lipoprotein(a) concentration of this population was 10.5 +/- 13.5 mg/dl and there was no significant difference between males and females (9.0 +/- 10.7 and 13.9 +/- 17.7 mg/dl, respectively). The distribution of plasma Lp(a) was highly skewed in the direction of low concentration values. In females a moderate bimodial distribution could be demonstrated. Documented by several authors lipoprotein(a) level higher than 30 mg/dl serves as an independent risk factor for atherosclerosis. In this population only 9.4% of subjects had lipoprotein(a) concentrations over this limit (5.9% female and 3.5% male). The relative alle frequency of different phenotypes showed the following distribution: B 0.007, S1 0.015, S2 0.154, S3 0.231, S4 0.230 and null 0.362. In this population the F phenotype could not be detected.
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PMID:[Plasma concentration of lipoprotein(a) and distribution of its subtypes in the healthy population of Hungary]. 214 42

Lipoprotein(a) [Lp(a)] is an extremely atherogenic lipoprotein. Lp(a) has been found in the plasma of humans and other primates, but until now only in a few other species. The mechanism by which it exerts its atherogenicity is still poorly understood. We observed that Lp(a) has been found in the plasma of several species unable to synthesize ascorbate and not in other species. We have now detected apoprotein(a) in the plasma of the guinea pig. We induced atherosclerosis in this animal by dietary ascorbate depletion and, using SDS/PAGE and subsequent immunoblotting, we identified Lp(a) as accumulating in the atherosclerotic plaque. Most importantly, adequate amounts of ascorbate (40 mg per kg of body weight per day) prevent the development of atherosclerotic lesions in this animal model and the accumulation of Lp(a) in the arterial wall. We suggest an analogous mechanism in humans because of the similarity between guinea pigs and humans with respect to both the lack of endogenous ascorbate production and the role of Lp(a) in human atherosclerosis.
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PMID:Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig. 214 14

The lipid that accumulates in some fibrous atherosclerotic lesions appears to be derived from plasma low density lipoprotein (LDL). An early stage in lipid accumulation may be immobilization of a fraction of the LDL, and this is released by incubation with proteolytic enzymes, of which the most effective is the fibrinolytic enzyme, plasmin. We have examined the relationship between release of fibrin degradation products (FDP) and LDL in controlled plasmin incubations of 42 samples of normal intima and atherosclerotic lesions from aortas of 10 patients. In three patients (group 1) no LDL was released from any of the 11 tissue samples although they comprised lesions as well as normal intima. In 2 more patients (group 2) LDL was consistently low. However, in 5 patients (group 3) substantial amounts of LDL were released from all 21 tissue samples, and there was a significant correlation between the amounts of FDP and LDL (P less than 0.001). In spite of this correlation there were marked differences in the ratio FDP/LDL, but analysis by SDS-polyacrylamide gel electrophoresis and immuno blotting of the FDP released showed no consistent pattern related to LDL binding. Although the ratio FDP/LDL showed a 4-fold range, in 6 lesions subjected to successive 2-h incubations with plasmin the ratio within each lesion remained constant, supporting the concept that fibrin and LDL are linked.
Atherosclerosis 1990 Oct
PMID:Factors influencing the accumulation in fibrous plaques of lipid derived from low density lipoprotein. I. Relation between fibrin and immobilization of apo B-containing lipoprotein. 214 67

Plasma lipids and apolipoproteins were quantified in two kindreds of hypobetalipoproteinemia. All affected members were asymptomatic but showed a decrease of 75% in apolipoprotein B and of 69% in LDL-cholesterol. There were no major changes in apo A-I and A-II but all affected family members had reduced levels of apo C-II (by 58%) and C-III (by 59%) without significant decrease in apo C-I and no specific decrease of apo C-III1. Apolipoprotein E is decreased in SDS-PAGE. The plasma level and phenotype of Lp(a) are not affected by HBL, suggesting that a catabolic rather than a synthetic mechanism is responsible for the disease. As shown by density gradient ultracentrifugation, HDL2 particles that contain essentially apolipoprotein A-I, cholesterol and phospholipids represent in affected subjects the major part of HDL. Due to the net reduction of apolipoprotein B-containing particles (VLDL and LDL) as acceptors of lipids in HBL, there is an accumulation of large particles rich in cholesteryl esters.
Atherosclerosis 1990 Aug
PMID:Plasma lipids, lipoproteins and apolipoproteins in two kindreds of hypobetalipoproteinemia. 224 96

Cultured fibroblasts from patients with familial hyperapobetalipoproteinemia (hyperapoB) were used to determine if a defect in lipid metabolism was present. Three basic proteins (BP I, BP II, and BP III) were isolated from normal human serum by preparative isoelectric focusing, preparative SDS/PAGE, and reversed-phase HPLC. The Mr and pI values of these proteins were 14,000 and 9.10 for BP I, 27,500 and 8.48 for BP II, and 55,000 and 8.73 for BP III. These proteins differed significantly in their content of arginine, cysteine, proline, histidine, serine, and methionine. BP I appears to be the same protein as acylation-stimulating protein, but BP II and BP III appeared different from acylation-stimulating protein and other lipid carrier proteins. BP I, BP II, and BP III stimulated the incorporation of [14C]oleate into lipid esters in normal fibroblasts, an effect that was time and concentration dependent. In hyperapoB cells, BP II markedly increased (up to 9-fold) the incorporation of [14C]oleate into cholesteryl ester compared with that in normal cells; in addition, there was a 50% decrease in the stimulation of triglyceride acylation and cholesterol esterification with BP I. No difference between normal and hyperapoB cells was observed with BP III. In summary, the identification of another serum basic protein, BP II, led to the elucidation of another cellular defect in hyperapoB fibroblasts, enhanced cholesterol esterification, which may be related to the precocious atherosclerosis and abnormal lipoprotein metabolism seen in hyperapoB.
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PMID:Acylation-stimulatory activity in hyperapobetalipoproteinemic fibroblasts: enhanced cholesterol esterification with another serum basic protein, BP II. 224 73

The types of collagen components extracted from human aortas by repeated pepsin digestion were investigated by SDS-polyacrylamide gel electrophoresis (SDS-PAGE), after differential salt precipitation, cyanogen bromide (CNBr) cleavage and beta-mercaptoethanol reduction. For further extraction of collagen components, repeated pepsin digestion was carried out, and two extracts, the former and latter, were obtained. The greatest increase was seen in type V collagen followed by type III in the former extract. Type I collagen was continually extracted, so the proportion of type I to other types became greater with the number of extractions. SDS-PAGE of the residue treated with CNBr revealed that it contained the greatest amount of type I, followed by the latter extract. Type I collagen comprised approximately two-thirds of the total collagen. It was the most predominant in the intima and adventitia but was also obviously abundant in the media. The proportion of type III collagen to total collagen fell slightly with advancing atherosclerosis, since the amounts of types I and V showed some increase. A band of the alpha 3(V) chain of type V collagen in the intima was occasionally detected between the bands of the alpha 1(V) and alpha 2(V) chains. Basement membrane collagen, type IV, which was extracted predominantly from the intima and subintima, showed a heterogenous distribution as to molecular size, ranging from 50 Kd to 140 Kd. The alpha 1(IV) and alpha 2(IV) collagens were found at positions corresponding to 100 Kd and 80 Kd, respectively. The content of collagen type IV also increased with the proliferative fibrotic process. Type VI collagen was found in the intima and subintima of the human aorta at a position corresponding to an approximate molecular weight of 150 Kd, and it was reduced to fragments of 40 Kd, 45 Kd and 52 Kd.
Atherosclerosis 1986 Jun
PMID:Collagen types in various layers of the human aorta and their changes with the atherosclerotic process. 308 34

The phenotype of smooth muscle cells (SMCs) in the aortic media of 7 human fetuses (14-20 weeks of gestation) was examined with transmission electron microscopy, immunofluorescence microscopy, and gel electrophoresis of the cytoskeletal and cytocontractile proteins. Ultrastructurally, virtually all medial cells were identified as SMCs having a poorly differentiated phenotype with a cytoplasm rich in rough endoplasmic reticulum and organelles, and with only a few myofilaments. All medial cells stained intensely with antibodies to vimentin, but only in a 20-week-old fetus could we find a few SMCs staining with antibodies to desmin. Nor was desmin detectable with SDS gel electrophoresis followed by immunoblotting, while clear bands corresponding to vimentin, myosin, and actin were present. In isoelectric focusing and two-dimensional gel electrophoresis beta-actin was the most prominent of the 3 actin isoforms in all cases. The present results show that SMCs in the media of fetal human aorta have a poorly differentiated phenotype, which morphologically and biochemically resembles that previously described in the aorta of fetal and newborn rat, in the arterial intima after endothelial injury, in atherosclerotic lesions, and after spontaneous modulation of medial SMCs in culture.
Atherosclerosis 1988 Nov
PMID:Characterization of the phenotype of smooth muscle cells in human fetal aorta on the basis of ultrastructure, immunofluorescence, and the composition of cytoskeletal and cytocontractile proteins. 321 79

Plasma low density lipoproteins (LDL) and/or other lipoproteins containing apo B that accumulate in atherosclerotic lesions of human aortas exhibit structural changes that are associated with enhanced uptake in an unregulated fashion by macrophages in culture, resulting in the formation of foam cells in vitro. In an attempt to better characterize the structure-function modifications, we have incubated plasma LDL with extracts of human atherosclerotic plaques obtained at surgery, and determined whether such plaque-modified LDL also demonstrates enhanced uptake by cultured mouse peritoneal macrophages (MPM). Enhanced uptake was found which was linear over a concentration range of 100 micrograms lipoprotein protein/ml, as assessed by enhanced degradation of [125I]LDL and by stimulation of cholesterol esterification. Extracts of non-arterial human tissue were unable to induce this modification, suggesting tissue specificity. When delipidated apo B from tissue-treated [125I]LDL was subjected to SDS-PAGE, autoradiograms demonstrated, in addition to the B-100 band of apo B, a doublet of higher molecular weight than B-100 and a band just entering the gel, both at the expense of the B-100 band. No lower molecular weight bands suggestive of apo B degradation were seen. Modest increases in LDL electrophoretic mobility and thiobarbituric acid reactive substances were found following the incubation of LDL with plaque extracts. These changes could be inhibited by butylated hydroxytoluene (BHT), suggesting that free radical-induced lipid peroxidation was responsible for these modifications. However, since BHT did not inhibit the uptake of the tissue-incubated LDL by macrophages, the actual modification responsible for enhanced macrophage recognition did not appear to be free radical-induced. Uptake of plaque-modified [125I]LDL was inhibited by only 22% by a 20-fold excess of acetyl LDL or plaque-modified LDL. If the latter did not represent a mixture of modified and unmodified particles, this result would suggest that uptake was not mediated by the scavenger receptor. It is possible that foam cells are formed in vivo when LDL particles, which have been modified by interacting with components of the arterial wall, are taken up by tissue macrophages.
Atherosclerosis 1988 Mar
PMID:Extracts of human atherosclerotic lesions can modify low density lipoproteins leading to enhanced uptake by macrophages. 335 15


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