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)

Lipoprotein (Lp)(a) concentrations were measured in eight patients with nephrotic syndrome in the age range of 8 to 69 yrs. Mean (+/- SE) levels of serum Lp(a) were elevated in the nephrotic patients compared to controls (76.5 +/- 19.7 vs 18.6 +/- 0.9 mg/dl, p less than 0.001). After treatment with prednisolone, Lp(a) concentrations were decreased from 85.2 +/- 21.6 to 42.2 +/- 14.0 mg/dl. During the treatment, serum total cholesterol showed a negative correlation with serum albumin concentration. However, no correlation was noted between Lp(a) and serum albumin concentration. There were no significant correlations between Lp(a) and other lipoprotein lipid and apolipoprotein levels. It was concluded that hyperLp(a)aemia may be an independent risk factor in the development of premature atherosclerosis in patients with nephrotic syndrome.
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PMID:A study of the clinical significance of lipoprotein (a) in nephrotic syndrome. 183 Sep 8

Serum low-density lipoprotein (LDL) concentration is a major determinant of susceptibility to the development of atherosclerosis. A major component of the protein moiety of LDL and its precursor very-low-density lipoprotein is apolipoprotein B (apo B). The human hepatoma cell line, Hep G2, was used as a model for the investigation of mechanisms which control hepatic secretion of the apo B and lipid components of lipoproteins. Using a sensitive immunoradiometric assay for apo B developed in this laboratory, we showed that bovine serum albumin inhibited and glucose, and fatty acids enhanced the rate of accumulation of apo B in the culture medium of Hep G2 cells. However, these substances did not necessarily affect LDL lipids in the same way as apo B. This finding appeared to be due to Hep G2 cells expressing lipase activities which led to triacylglycerol and phospholipid hydrolysis and lipid reuptake. Reuptake of apo B also occurred, but its rate of accumulation in the culture medium suggested it was a closer reflection of its true secretory rate.
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PMID:Lipoprotein secretion by the human hepatoma cell line Hep G2: differential rates of accumulation of apolipoprotein B and lipoprotein lipids in tissue culture media in response to albumin, glucose and oleate. 195 47

Fibrinolytic system, immune reactivity and isoelectric focusing of serum albumin were examined in 94 patients exhibiting combination of obstructive lung disease (chronic obstructive bronchitis and bronchial asthma) with atherosclerosis. Plasminogen activator showed discrete activity, the discreteness being less in respiratory distress of the I degree but higher in the distress of the II and III degree. Relative number of E-RFC and monocytes expressing receptors to IgM and IgG Fc-fragment decreased. Percentage of EAC-RFC rose. Serum albumin fractions changed pH range due to modification of albumin molecules resultant from forming complexes with fibrinogen degradation products. Concentration of the latter under conditions of respiratory distress induced by obstructive lung diseases associated with atherosclerosis substantially exceeded the standard levels.
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PMID:[Fibrinolysis, immune reactivity and the structure of the blood serum albumin in obstructive lung diseases combined with atherosclerosis]. 207 78

The amount of cholest-5-en-3 beta,7 beta-diol (CD) was significantly higher in cultures of human monocytes incubated with cholesteryl linoleate-bovine serum albumin (CL/BSA) artificial lipoproteins than in no-cell control incubations of CL/BSA. CD production by monocytes was almost completely inhibited by the radical scavengers butylated hydroxytoluene (BHT), probucol, and alpha-tocopherol, and was partially inhibited by the metal chelator EDTA. The production of CD was accompanied by decrease in linoleic acid. CD amounts were negligible in incubations of monocytes with cholesteryl oleate/BSA (CO/BSA) or cholesterol/BSA (C/BSA). Ability to produce CD from CL/BSA appeared to increase with age in culture of human monocyte-macrophages. Considerable variations were observed in the CD production from CL/BSA by monocytes from different blood donations. Higher levels of CD production appeared more common with monocytes from men than from women. The significance of these results in the context of human atherosclerosis is discussed.
Atherosclerosis 1990 Aug
PMID:Oxidation of cholesteryl linoleate by human monocyte-macrophages in vitro. 212 6

The progressive microcirculatory changes caused by hypercholesterolemia were studied in the rat cremaster model by use of intravital microscopy. Male Sprague-Dawley rats were fed either a normal chow diet or a chow diet supplemented with 1% cholesterol and 0.5% cholic acid for 1, 3, or 5 wk before experimentation. After 3 wk on the diet, hypercholesterolemia produced a significantly decreased vasoconstrictor response to norepinephrine in both arterioles and venules. After 5 wk, there was also significantly reduced macromolecular leakage induced by exogenous histamine and compound 48/80 in the high-cholesterol group. However, there was no change in the degree of base-line macromolecular leakage. Platelet thrombi formation induced by light activation of intravascular fluorescein isothiocyanate tagged to bovine serum albumin was slightly increased by hypercholesterolemia. Despite these microcirculatory changes there was no microscopic evidence of atheromatous pathology after 5 wk on the cholesterol diet. These results suggest a progressive nonspecific receptor desensitization and decreased inflammatory response shortly after the initiation of elevated serum cholesterol but before any histological evidence of atherosclerosis.
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PMID:Progressive microcirculatory changes caused by hypercholesterolemia in rats. 233 80

Mouse resident peritoneal macrophages (MPM) cultured with artificial lipoprotein consisting of cholesteryl linoleate complexed with bovine serum albumin (CL/BSA) rapidly accumulate ceroid in the form of rings. Experiments with various phenolic radical scavenger antioxidants and derivatives showed that the radical scavengers which are strongly lipophilic, and possess a free (i.e. non-esterified) phenolic hydroxyl group are inhibitors of ceroid ring formation. Time-course experiments with MPM and CL/BSA in which either or both of the components of the artificial lipoprotein have been oxidised before feeding showed that such oxidation accelerated ceroid accumulation, and suggested that oxidation of the lipoprotein is rate-determining in ceroid accumulation. Copper appeared to be a good catalyst for this. Agents able to activate the respiratory burst production of reactive oxygen species appeared to have no accelerating effect on ceroid accumulation from CL/BSA by MPM in a time-course. A novel method has been attempted for quantitating ceroid in MPM by means of its autofluorescence, using a Fluorescence-activated Cell Sorter (FACS). The results from FACS agree qualitatively with those from alcohol-xylene treatment followed by oil-red-o staining (AX/ORO). MPM cultured with CL/BSA for up to 4 days showed a 2.7-4.6-fold increase in mean fluorescence (at wavelengths greater than 490 nm) over MPM cultured with cholesteryl oleate/BSA (CO/BSA), with CL/BSA/butylated hydroxytoluene (CL/BSA/BHT), with CL/BSA/probucol, and with no artificial lipoprotein. The implications of the findings with respect to human atherosclerosis are discussed.
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PMID:Modulation of ceroid accumulation in macrophages in vitro. 248 61

Low density lipoproteins (LDL) that have been oxidatively modified have been implicated in the pathogenesis of atherosclerosis. Monoclonal antibodies were generated against oxidatively modified human low density lipoproteins (OxLDL); these antibodies reacted with OxLDL, but did not react with native LDL, either in an enzyme-linked immunosorbent assay (ELISA) or a Western blot analysis. The anti-OxLDL antibodies did react with other modified forms of LDL (eg, acetylated LDL, malondialdehyde-modified LDL, and cell-modified LDL) that were recognized by the scavenger receptor on macrophages. Single- and double-label immunofluorescence of atheromatous lesions from a Watanabe heritable hyperlipidemic (WHHL) rabbit demonstrated some colocalization of proteins detected by anti-LDL and anti-OxLDL antibodies. However, clearly there were also areas stained by the anti-OxLDL antibodies that did not stain with anti-LDL. Staining of the lesion by the anti-OxLDL antibody was abolished by adsorption of the antibody with OxLDL, but not by adsorption with LDL or bovine serum albumin. Arterial tissue from a control New Zealand White rabbit did not show staining with anti-LDL or anti-OxLDL antibodies. These observations suggest that OxLDL (or possibly other proteins recognized by the anti-OxLDL antibody) is present in atheromatous lesions of WHHL rabbits, and are consistent with oxidatively modified lipoproteins having a role in atherogenesis.
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PMID:Direct evidence for a protein recognized by a monoclonal antibody against oxidatively modified LDL in atherosclerotic lesions from a Watanabe heritable hyperlipidemic rabbit. 268 96

The utility of nonspecific polyclonal IgG for external imaging of experimental atherosclerosis was tested in a series of rabbits after balloon catheter deendothelialization of the abdominal aorta. Following injection of 111In-IgG, 111In-Fc, or 111In-Fab serial images were recorded. In addition, several animals received 125I-low density lipoproteins [125I-LDL], or 125I human serum albumin [125I-HSA] as positive and negative controls. Forty-eight hours after injection of the radiolabeled proteins, the aortas were removed, divided into abdominal and thoracic regions, counted, and autoradiographed. The images acquired after injection of 111In-IgG and 111In-Fc, showed clear focal accumulation of radioactivity in the healing abdominal aorta. In contrast, the images obtained after injection of 111In-Fab did not show focal radionuclide accumulation. For 111In-IgG and 111In-Fc there were three to six times as many counts in the abdominal as in the thoracic aorta, while for 111In-Fab and 125I HSA, the abdominal and thoracic counts were nearly equal. The results suggest that radiolabeled IgG and Fc can be used to image experimental atherosclerosis.
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PMID:Radionuclide imaging of experimental atherosclerosis with nonspecific polyclonal immunoglobulin G. 273 90

Lecithin:cholesterol acyltransferase (LCAT) and lysolecithin acyltransferase (LAT) are two activities carried out by the same plasma enzyme, but require different apoprotein activators. The LCAT reaction takes place primarily on high density lipoproteins (HDL) and is activated by serum albumin, whereas LAT takes place on low density lipoproteins (LDL) and is inhibited by albumin. In nephrotic syndrome (NS), the levels of serum albumin are reduced, whereas the LDL levels are increased, and therefore, the ratio of LAT/LCAT activities should be increased. To test this hypothesis, we estimated the lipid levels and the two enzyme activities in experimental NS induced in rats by the injection of anti-Fx1A antibody (passive Heymann nephritis). As found in other nephrotic conditions, the plasma lipid levels rose progressively as the proteinuria increased and the serum albumin concentration declined. In addition, the ratio of LAT/LCAT activities increased by about fourfold after nine days of induction of nephritis. The LCAT activity correlated positively and the LAT activity negatively with serum albumin levels. The esterified cholesterol correlated positively with LCAT activity in normal rats but negatively in nephrotic animals, indicating that most of the cholesteryl esters in NS may be non-LCAT derived. The free cholesterol/lecithin ratio, a known risk factor for atherosclerosis, increased significantly in nephrotic rats. Furthermore, since the increase in the LAT activity produces more disaturated lecithins, another putative risk factor, the cumulative risk of coronary heart disease may be increased in long-term NS.
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PMID:Plasma lipids and acyltransferase activities in experimental nephrotic syndrome. 277 94

The morphologic, biochemical, and mechanical abnormalities of connective tissue fibrous proteins in Marfan's syndrome have been well studied, and their role in cardiovascular complications is well accepted. Less is known, however, about the state of the amorphous components of the aortic connective tissue. In the course of a study of transmural transport in blood vessels, we have had the opportunity to study dystrophic aorta from two young men who survived elective surgery; both with aortic insufficiency (AI) histologically compatible with Marfan's syndrome. One had recurrent chronic dissecting aneurysm (RCDA) as well. The aorta of the first (but not the second) was histologically compatible with Marfan's syndrome. Fresh specimens of intact ascending aorta were incubated in Krebs solution, pH 7.4, containing 125I-labelled bovine serum albumin for 2 h at 37 degrees C. The samples were then frozen, and serially sectioned in the plane of the lumenal surface. The radioactivity of the 20-micron thick sections was then determined, and expressed as a tissue/labelled solution concentration ratio. Transmural profiles of these ratios revealed no difference between the aorta of the RCDA patient with non-specific aortic dystrophy, and that of a 70-year-old man undergoing aortocoronary bypass. However, in the patient with aortic histology compatible with Marfan's syndrome, the average media concentration ratio was 5-fold less (4% vs. 20%).
Atherosclerosis 1988 Sep
PMID:Aortic 125I-albumin transport in patients with Marfan's syndrome and annuloaortic ectasia. 317 29


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