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)

LDL (0.5 - 2.0 mg LDL-cholesterol/ml) isolated from venous blood of healthy male volunteers stimulated dose-dependently the malondialdehyde (MDA) formation by frozen human platelets, used as a marker for the activity of the thromboxane synthetase. HDL (0.25 - 1.0 mg HDL-cholesterol/ml) and human serum albumin (1 - 10 mg/ml) had no concentration-dependent influence on the MDA formation. If these results can be extended to in vivo they suggested the strong connection between the prostaglandin and lipoprotein hypothesis of pathogenesis of atherosclerosis.
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PMID:Low density lipoprotein (LDL) from male volunteers stimulated the thromboxane formation by human platelets. 657 27

The effect of immune complexes on plasma lipids, especially on high density lipoprotein (HDL) cholesterol, was studied in rabbits. In rabbits immunized twice with bovine serum albumin (BSA) with an interval of about 6 weeks, a significant decrease in plasma HDL-cholesterol (P less than 0.01) and in the HDL/total cholesterol ratio (P less than 0.02) was found 6 days after the second BSA injection. As a result of repeated bleedings commenced 6 days after the second BSA injection, the changes in plasma triglycerides (TG) and total cholesterol (TC) were similar to those found previously in non-immunized rabbits. In contrast to the findings in non-immunized rabbits, no significant decrease in HDL-cholesterol was found as a consequence of the bleedings, but a negative correlation (P less than 0.05) between plasma TG and HDL-cholesterol appeared. It is concluded that immune complexes may affect plasma HDL-cholesterol concentrations and thereby possibly also the development of atherosclerosis.
Atherosclerosis
PMID:Effect of immune complexes on plasma HDL-cholesterol in rabbits. 722 78

The effect of immune complexes on plasma lipids, especially triglycerides (TG) was studied in rabbits. After a single intravenous dose of bovine serum albumin (BSA), serological aberrations suggestive of immune complexes appeared around the 14th day. Changes in the plasma TG or cholesterol values were not observed within a follow-up period of 4 weeks. However, reimmunization with a second dose of BSA 2 months later led to a significant decrease in plasma TG (P less than 0.01). In fat tolerance tests TG emulsion was given intravenously to rabbits immunized 14 days earlier with BSA. The elimination curve of exogenous TG (followed for 100 men) was in its first phase exponential and in it second phase linear in all experimental groups. The significance of the second phase, however, has to be interpreted with some caution because of the possible recirculation of TG into the blood stream. In the rabbits immunized with one dose of BSA the fractional removal rate of TG did not differ from that of the controls. However, in the rabbits reimmunized with a second dose of BSA 2 months later the fractional removal rate of TG was greater than in the controls (P less than 0.01). It was concluded that immune complex lesions under certain circumstances may affect the TG metabolism. The mechanism concerned may be increased permeability of the injured vascular endothelial cells, possibly through the increased release of lipoprotein lipase (LPL).
Atherosclerosis 1980 Apr
PMID:Effects of immune complexes on plasma triglycerides in rabbits. 737 24

We examined the relation between in vivo thrombogenicity and the morphology of carotid lesions to clarify the role of platelet deposition in carotid atherothrombosis. We evaluated 60 subjects (120 carotid bifurcations) who had at least one established risk factor for atherosclerosis by using indium 111 platelet scintigraphy and high-resolution B-mode ultrasonography. We evaluated platelet accumulation in the carotid arterial wall by means of a dual-tracer method that used In 111-labeled platelets and technetium 99m-labeled human serum albumin. The tracer accumulation was assessed both visually and semiquantitatively by using the platelet accumulation index, ie, the ratio of radioactivity of the amount of In 111-labeled platelets deposited on the vascular wall to the amount of radioactivity in labeled platelets circulating in the blood pool. The morphology of the carotid lesions was analyzed with B-mode ultrasonography in terms of the presence of ulceration, the maximum percent stenosis, the echogenicity of plaque, and the plaque score, which indicates the severity of systemic atherosclerosis. Platelet accumulation increased with increase in plaque score (P < .01), and the magnitude of platelet accumulation was significantly greater in lesions with ulceration than in those without (P < .05). The platelet accumulation index in vessels with plaque showed a very weak but significant correlation with maximum percent stenosis (r = .28, P < .05) and a stronger correlation with the unilateral plaque score (r = .42, P < .0001). Analysis of the echogenicity of plaque showed that heterogeneous plaque had a high frequency of accumulating platelets. Platelet accumulation was related to the surface characteristics and severity of carotid lesions, especially in the presence of ulceration.
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PMID:Functional and anatomic evaluation of carotid atherothrombosis. A combined study of indium 111 platelet scintigraphy and B-mode ultrasonography. 748 48

Oxidation of LDL is thought to contribute to the early stages of atherogenesis. Because myeloperoxidase is present in atherosclerotic lesions and can produce the strong oxidant hypochlorous acid (HOCl), which converts LDL into its high-uptake atherogenic form in vitro, we raised polyclonal and monoclonal antibodies (MoAbs) against HOCl-modified LDL (HOCl-LDL). Characterization of the polyclonal anti-human HOCl-LDL Abs showed that they cross-reacted strongly with 4-hydroxynonenal-, malondialdehyde-, and Cu(2+)-oxidized LDL. Similarly, polyclonal and some monoclonal Abs against aldehyde- and Cu(2+)-modified LDL cross-reacted with HOCl-LDL. In contrast to the polyclonal Abs, two selected hybridoma cell line supernatants containing MoAbs raised against HOCl-LDL (MoAb-A and MoAb-B) did not cross-react with either native LDL or aldehyde- or Cu(2+)-modified LDL. MoAb-A (clone 1B10A11, subtype IgG1 kappa) recognized an epitope that appeared to be specific for HOCl-LDL and depended on the tertiary structure of the (lipo)protein, as judged by a lack of cross-reactivity with HOCl-modified human and bovine serum albumin and a loss of reactivity associated with lipoprotein denaturation. MoAb-B (clone 2D10G9, subtype IgG2b kappa), on the other hand, gave identical titration curves with HOCl-LDL and HOCl-modified albumins, suggesting that this antibody recognized epitopes that are commonly generated on proteins that have been oxidized with HOCl. Thus, MoAb-A and MoAb-B may be useful tools for the investigation of a possible role for HOCl-mediated damage to (lipo)proteins in atherosclerosis and other inflammatory diseases.
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PMID:Immunologic detection and measurement of hypochlorite-modified LDL with specific monoclonal antibodies. 754 Dec 96

A prominent feature of human atherosclerosis is the lipid-laden foamy macrophage, which often also contains the insoluble pigment, ceroid. The culture of macrophage-like cells, P388D1s, with artificial lipoproteins composed of cholesteryl linoleate (CL) and bovine serum albumin (BSA) results in foam cell formation with lipoprotein uptake and the intracellular accumulation of ceroid. Ceroid accumulation is accompanied by the oxidation of the cholesterol ester as monitored by gas chromatography. The sodium salt of diethyldithiocarbamic acid (DDC) at 1-5 microM effectively inhibited lipoprotein uptake, cholesteryl linoleate oxidation and ceroid accumulation in cultures of P388D1. Further studies showed that intracellular ceroid accumulation appeared to require the presence of cystine in the medium. Lipoprotein oxidation by this macrophage-like cell therefore appears to involve a mechanism dependent on cystine metabolism which is consistent with previous reports of macrophage-mediated lipoprotein oxidation. Studies on CL/BSA-induced ceroid accumulation in human monocytes also showed that DDC behaved in much the same manner. This inhibitory effect of DDC on foam cell formation, often considered a primary event of atherosclerosis, at concentrations as low as 1 microM, suggests the need for further, more comprehensive, studies on this compound's activities.
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PMID:The inhibition of foam cell formation by sodium diethyldithiocarbamate. 758 21

We examined the association of serum albumin concentration with diabetes mellitus and other cardiovascular risk factors, prevalent cardiovascular disease, and ultrasonographically assessed carotid artery intima-media thickness using data from 45- to 64-year-old adults in the Atherosclerosis Risk in Communities (ARIC) Study. The mean albumin concentration was 0.04 to 0.12 g/L lower in participants with diabetes and 0.02 to 0.06 g/L lower in those with cardiovascular disease, compared to participants without these conditions. However, lower serum albumin level was also correlated with most traditional risk factors and hemostatic variables. On adjustment for these, there was essentially no association between serum albumin and prevalent cardiovascular disease. Likewise, there was no association between albumin and carotid intima-media thickness (a marker of atherosclerosis). While hypoalbuminemia may be a marker for chronic disease and perhaps renal loss of albumin, it seems unlikely that it is an important cause of atherosclerosis.
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PMID:Low serum albumin. Association with diabetes mellitus and other cardiovascular risk factors but not with prevalent cardiovascular disease or carotid artery intima-media thickness. The Atherosclerosis Risk in Communities (ARIC) Study Investigators. 760 7

Modification of proteins by long-term incubation with glucose leads to the formation of advanced glycation end products (AGE). Recent immunological demonstration of the presence of AGE proteins in several human tissues suggests that they may be involved in aging, diabetic complications and atherosclerosis. AGE proteins are taken up by macrophages via the AGE receptor, which is similar to the macrophage scavenger receptor (MSR). In the present study, we examined whether MSR could mediate the endocytic uptake of AGE proteins by using Chinese hamster ovary (CHO) cells overexpressing bovine type II MSR (CHO-SRII). 125I-labelled AGE bovine serum albumin (125I-AGE-BSA) as well as 125I-acetylated low-density lipoprotein (125I-acetyl-LDL) underwent endocytic degradation by CHO-SRII cells, but not by control CHO cells. Endocytic degradation of 125I-acetyl-LDL and 125I-AGE-BSA by CHO-SRII cells was significantly inhibited by unlabeled AGE-BSA, as well as by acetyl-LDL. Immunoelectron microscopic studies using both AGE-BSA conjugated with gold particles and anti-(bovine MSR) antibody (D2) revealed co-localization of gold particles and the reactive sites for the antibody at coated pits of plasma membranes as well as in endosomes. These results clearly show that MSR mediates the endocytic uptake and degradation of AGE proteins, suggesting a new role of MSR in biological recognition of AGE in vivo.
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PMID:Macrophage scavenger receptor mediates the endocytic uptake and degradation of advanced glycation end products of the Maillard reaction. 760 9

A chondroitin sulfate-dermatan sulfate proteoglycan was isolated from bovine aorta intima by extraction of the tissue with 4 M guanidine hydrochloride. The proteoglycan was purified by CsCl isopycnic centrifugation followed by gel filtration and ion exchange chromatography. A monoclonal antibody C8F4 was developed to this core protein. The characteristics and specificity of the antibody were studied by an enzyme-linked immunosorbent assay (ELISA) using an alkaline phosphatase conjugated antibody (goat anti-mouse IgG). The antibody binding to the core protein was found specific and optimal at pH 7.0. The antibody recognizes either intact chondroitin sulfate-dermatan sulfate proteoglycan monomer, chondroitinase ABC digested monomer or chemically deglycosylated proteoglycan. Free chondroitin sulfates, keratan sulfate and hyaluronic acid did not compete for the antigenic sites in ELISA. Limited hydrolysis of the core protein by trypsin resulted in three peptides and only the peptide with a molecular weight M(r) = 40,000 was found capable of binding to hyaluronic acid. The antibody C8F4 recognized this hyaluronic acid binding peptide but did not recognize the other two peptides suggesting that the epitope(s) for this antibody is in the hyaluronic acid-binding region of the core protein. The antibody recognized the core proteins from bovine nasal cartilage proteoglycan and human aorta proteoglycan but did not recognize bovine aorta link protein, bovine serum albumin, human serum albumin, human transferrin, collagen Type I and fibronectin. The antibody was found useful to localize proteoglycans in atherosclerotic lesions in human aorta by immunohistochemical techniques.
Atherosclerosis 1993 Jan 25
PMID:A monoclonal antibody that recognizes hyaluronic acid binding region of aorta proteoglycans. 768 Dec 90

We previously reported that oleic acid (OA) rapidly increased apolipoprotein (apo) B secretion by suppressing early intracellular degradation of nascent apo B in Hep G2 cells and suggested that the suppression of apo B degradation is associated with triglyceride (TG) biosynthesis from OA. To determine whether the inhibition of apo B degradation is associated with increased TG synthesis or is a direct effect of OA, we examined the effect of another fatty acid, eicosapentoenoic acid (EPA), on apo B kinetics in Hep G2 cells, since it is well known to have hypolipidemic action in clinical studies. The incorporation of [3H]glycerol into cellular TG was stimulated five-fold when Hep G2 cells were incubated for 2 h with EPA or OA (0.4 or 0.8 mM-1.5% bovine serum albumin (BSA) complex). The incorporation of [14C]acetic acid into cellular cholesteryl ester (CE) was significantly decreased by EPA treatment, whereas OA did not affect CE synthesis. Similar effects of these fatty acids on cellular lipid synthesis were observed in long-term incubation (24 h). Apo B was linearly secreted into the medium during 3 h, and EPA and OA doubled the rate of secretion. In long-term (24 h) incubations, both fatty acids significantly increased the incorporation of [3H]leucine into secreted apo B radioactivity or the accumulation of apo B mass in the medium. Pulse-chase studies revealed that both EPA and OA reduced intracellular apo B degradation to a similar degree. The inhibition of apo B degradation was also observed when the cells were preincubated with either EPA or OA for 24 h. These results suggest that increased TG synthesis leads to suppression of intracellular apo B degradation, which is independent of the source of exogenous fatty acid.
Atherosclerosis 1995 Jan 06
PMID:Similar to oleic acid, eicosapentaenoic acid stimulates apolipoprotein B secretion by inhibiting its intracellular degradation in Hep G2 cells. 777 67


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