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)

A number of soluble proteins contained in human aortic intimal tissue was extracted into buffered saline (pH 7.4) and identified and quantitated by immunoelectrophoresis and immunodiffusion. The proteins included IgA, IgG, IgM, B1C (C3), alpha 1-antitrypsin, alpha 2-macroglobulin, fibrinogen, albumin, LDL, HDL, alpha 1-acid glycoprotein, beta 2-glycoprotein, transferrin and ceruloplasmin. The concentration of soluble proteins was significantly higher in the atherosclerotic intima than in the normal intima. The diseased intima also contained a small amount of tissue-bound IgG, IgA and B1C which was extractable with citrate buffer at pH 3.2. The vascular band IgG, and B1C were shown by enzymatic and immunohistochemical studies to be closely associated with the collagenous tissue of the plaque. The Ig contained in the atherosclerotic plaque may be derived in part from the biosynthesis of Ig by the artery, since the incorporation of 14C-labeled leucine into IgG by the atheromatous plaque was demonstrable by radioimmunoelectrophoresis. In contrast to the diseased artery, the normal artery did not synthesize IgG and did not contain vascular bound IgG or complement. However, the normal artery was capable of fixing IgG and B1C eluted from the diseased artery. The present studies suggested that the IgG contained and synthesized by the plaque might represent an immune response to an endogenous or exogenous antigen closely associated with plaque collagen. IgG and B1C either alone or in the form of an immune complex also may play an important role in phagocytosis in the plaque and thereby influence the course of atherosclerosis. The proteolytic inhibitors, alpha 1-antitrypsin and alpha 2-macroglobulin, found in relatively high concentrations in the plaque, could enhance fibrosis of the lesion because of thier known inhibitory effects on collagenase and elastase.
Atherosclerosis 1979 Dec
PMID:Soluble proteins in the human atherosclerotic plaque. With spectral reference to immunoglobulins, C3-complement component, alpha 1-antitrypsin and alpha 2-macroglobulin. 9 93

The effect of nicotinic acid was investigated in Rhesus monkeys. Subcutaneous injections of nicotinic acid lower the plasma very low density lipoprotein (VVLDL) and low density lipoprotein (HDL) concentration. The fall in LDL concentration is not accompained by any change in the lipid or protein composition of either lipoprotein. Analysis by Sephadex gel chromatography and polyacrylamide-gel electrophoresis showed that the proteins of monkey VLDL and LDL are qualitatively similar to those of human VLDL and LDL, although there are differences in the proportions of the various proteins present in the two species. Subcutaneous injections of nicotinic acid diminish the maximum incorporation of 14C from [14C]threonine into VLDL and LDL apoproteins, but have no effect on incorporation into albumin or HDL apoprotein. Peak incorporations into the apo-B and apo-C of VLDL are diminished to about equal extents by nicotinic acid. Comparison of the amount of 14C lost from apo-B of VLDL after the peak of incorporation, with that gained by apo-B of LDL during the same period, suggests that some of the circulating apo-B of LDL IS DERIVED FROM SOURCES OTHER THAN CIRCULATING VLDL.
Atherosclerosis
PMID:The effect of nicotinic acid on the metabolism of the plasma lipoproteins of rhesus monkeys. 16 24

Plasma lipids and chemical, electrophoretic and electron microscopic properties of VLDL, LDL and HDL are examined in rabbits fed a control diet (group I) or diets containing 1% cholesterol (group II), 1% cholesterol + 5% coconut oil (group III) or 1% cholesterol + 5% corn oil (group IV). The diets II, III and IV resulted in hypercholesterolemia, hypertriglyceridemia and hyperphospholipidemia. The lipid-protein composition of VLDL, LDL and HDL is changed by these diets. There is marked increase in the total cholesterol content of all lipoprotein fractions of the high fat dietary groups II, III and IV. The electrophoretic mobilities of the VLDL and LDL II and III are reduced while the respective mobilities in the corn oil group IV are nearly "normal". In contrast to the control LDL fraction I which is not precipitated by heparin, the LDL fractions of the dietary groups II, III and IV are readily precipitated. The apoprotein pattern of the lipoproteins in polyacrylamide gel differs distinctly between the dietary groups, most bands appearing in group IV. An abnormal stacking of lipoprotein particles in electron micrographs of VLDL, LDL and HDL of groups II and III can be observed. In contrast, these lipoprotein fractions of rabbits of the corn oil group IV have morphological properties that are similar to those of the lipoproteins of the control group. It is suggested that these findings are related to the marked reduction of atherosclerosis in rabbits fed a diet with polyunsaturated fat as compared with rabbits on cholesterol and cholesterol-coconut oil diets.
Atherosclerosis
PMID:Changes in rabbit lipoprotein properties by dietary cholesterol, and saturated and polyunsaturated fats. 16 9

In one family the mother, two children and a maternal aunt showed a hypercholesterolemic state characterized by a unusually high percentage of cholesterol in ultracentrifugally-recovered HDL-(a)-LP. An intensely stained a-band was present in all these subjects both in plasma and in ultracentrifugal fraction, with d greater than 1063. Symptoms or signs due to the hypercholesterolemic state were not present. The father was affected by Type IIA hypercholesterolemia. This lipid defect was also present in one of the two children.
Atherosclerosis
PMID:Familial hyper-HDL-(a)-cholesterolemia. 16 11

Pig plasma lipoproteins were separted into four density classes (very low density, two low density and high density lipoproteins, VLDL, LDL1, LDL2 and HDL respectively) from 670 ml plasma by ultracentrifugation in a continuous density gradient using the Spinco Ti15 zonal rotor. LDL1 and LDL2 were partly characterised. LDL1 and LDL2 are beta-migrating lipoproteins of different size and hydrated density; they are similar to human LDL2 and LDL3 respectively. Pig plasma contains about twice as much LDL1 as LDL2. LDL1 migrates at Sf 4.9 (modal value), and has a mean diameter of 217 A and a modal density of 1.035 g/ml (range 1.03-1.04 g/ml). LDL2 migrates at Sf 1.8 and has a mean diameter of 195 A and a density of 1.050 g/ml. Both lipoproteins are precipitated by heparin and Mn++ or by dextran sulphate and Ca++. The apoproteins of LDL1 and LDL2 are both largely insoluble in 8 M urea solution. When dissolved in 1% sodium dodecyl sulphate solution and electrophoresed on polyacrylamide gel at pH 7.0, the apoproteins of LDL1 and LDL2 formed a pattern of multiple bands of high molecular weight similar to that obtained from the apoprotein of human LDL. Both LDL1 and LDL2 share a major antigen with each other and with VLDL; in this respect again they resemble human LDL. The amino acid compositions of LDL1 and LDL2 are very similar. We concluded that the apoprotein moieties of pig plasma LDL1 and LDL2 are probably identical, and similar to apoprotein B in human serum. Zonal ultracentifugation has proved to be a rapid and effective method for isolating large quantities of these two lipoprotein classes for further metabolic studies. This method allows rapid bulk preparation of lipoproteins, and provides a record of their distribution and quantity in a continuous density gradient.
Atherosclerosis
PMID:Properties of two pig low density lipoproteins prepared by zonal ultracentrifugation. 17 55

The plasma concentration of unesterified and esterified cholesterol within very low density (VLDL), low density (LDL) and high density (HDL) lipoproteins have been examined in relation to the metabolism and pool size of cholesterol in normal and hyperlipidaemic subjects. Cholesterol metabolism was assessed as faecal endogenous neutral and acidic steroid excretion, a 2-pool model of cholesterol turnover, and in vitro plasma cholesterol esterifying activity. VLDL total cholesterol (TC) concentration was positively correlated with cholesterol turnover, endogenous neutral steroid excretion, bile acid excretion and the absolute rate of plasma cholestrol esterification. The correlations with cholesterol turnover and neutral steroid excretion, but not that with bile acid excretion, remained significant when these were corrected for their relationships to body weight. LDL-TC was negatively correlated with the fractional rate of plasma cholesterol esterification and, in subjects with primary type IIa hyperlipoproteinaemia, also with the rate constant for cholesterol elimination from the rapidly exchanging cholesterol pool. No correlation was found between LDL-TC concentration and bile acid excretion. HDL-TC concentration was negatively correlated with both the rapidly and slowly exchanging pools of tissue cholesterol, after correction for their relationships to body weight and adiposity. In contrast, cholesterol pool sizes were not correlated with the concentration of VLDL or LDL-TC; nor was there any relationship to plasma cholesterol esterifying activity. No correlation was found between the relative proportions of unesterified cholesterol within any lipoprotein fraction and either the pool size or metabolism of cholesterol. These findings accord with previous reports of enhanced cholesterol metabolism in subjects with elevated VLDL concentrations and of impaired plasma LDL and cholesterol clearance in patients with primary type IIa hyperlipoproteinaemia. The demonstration that HDL-TC concentration is negatively correlated with body cholesterol pool size supports in vitro evidence for a role of HDL IN TISSUE CHOLESTEROL CLEARENCE.
Atherosclerosis
PMID:Relationships between plasma lipoprotein cholesterol concentrations and the pool size and metabolism of cholesterol in man. 17 28

(1) Male turkey serum contains two major lipoprotein families designated as LP-A and LP-B in its lipoprotein density classes. These two lipoprotein families were separated from each of the lipoprotein density classes by affinity chromatography on concanavalin A-Sepharose 4B. LP-A was present in the unretained and LP-B in the retained fractions. Both lipoprotein families were characterized by determination of their immunological and electrophoretic properties, the flotation coefficient and chemical composition. (2) LPb was distributed over a wider density range than LP-A. Seventy-four percent of LP-B was found in the LDL, 17% IN The VLDL and 8% in the HDL. In contrast, 98% of LP-A was present in the HDL and 2% in the LDL fractions: there were only trace amounts of LP-A in the VLDL. (3)Immunological and electrophoretic studies showed that the protein moiety of LP-A contained only the two non-identical A-I and A-II polypeptides of ApoA. The protein moiety of LP-B consisted only of ApoB. (4) Isolation of LP-A and LP-B from the major lipoprotein density classes provided further experimental evidence to confirm the existence of chemically distinct lipoprotein families as the fundamental physical-chemical entities of the serum lipoprotein system.
Atherosclerosis
PMID:Lipid transport in the avian species. Part 2. Isolation and characterization of lipoprotein A and lipoprotein B, two major lipoprotein families of the male turkey serum lipoprotein system. 18 84

(1) Lipoproteins from the serum of male turkeys maintained on a normal diet were separated by sequential preparative ultracentrifugation into VLDL (d less than 1.006 g/ml), LDL (d = 1.006-1.063 g/ml), HDL (d = 1.063-1.21 g/ml) and VHDL (d greater than 1.21 g/ml). Lipoprotein density classes were characterized by analytical ultracentrifugation, agarose electrophoresis, immunodiffusion and immunoelectrophoresis, and by quantitative determination of protein, lipids and individual phosphatides. (2) HDL were the major density class representing 75% of the total lipoprotein content, LDL accounted for approximately 20% and VLDL for only 3-5% of the total lipoproteins. (3) VLDL were characterized by a relatively low content of glyceride (34%). Cholesterol esters were the major lipid (38%) of LDL, and the phospholipids (26%) of HDL. Glycerides of all major density classes consisted of equal amounts of triglycerides and diglycerides. (4) Phosphatidylcholine was the major phosphatide in all density classes. The composition of phosphatides was very similar in the VLDL and LDL, but it was different in the HDL. The ratio of phosphatidylcholine/sphingomyelin was higher in HDL than in VLDL and LD. (5) Immunological and electrophoretic studies showed that all three major density classes consisted of two lipoprotein families designated, in analogy to the human serum lipoprotein system [1], as LP-A and LP-B. The exception was HDL3 (d = 1.125-1.21 g/ml) which contained only LP-A. (6) ApoB was insoluble in aqueous buffers but could be solubilized after reduction and carboxymethylation. No C- or N-terminal amino acids were released by the usual chemical methods. The carbohydrate moiety of ApoB contained mannose, galactose and galactosamine. (7) ApoA consisted of a non-identical polypeptides designated in analogy to the human polypeptides as A-I and A-II. A-I was the major ApoA polypeptide and had a molecular weight of about 27,000. This polypeptide contained no half cystine, and the aspartic acid as the N-terminal and alanine as the C-terminal amino acids. A-II had a molecular weight of about 10,000, contained no half cystine and had alanine as the C-terminal amino acid. A-II showed no N-terminal amino acid by either dansylation, dinitrophenylation or Edman's procedure. Neither A-I nor A-II contained neutral sugars or hexosamines. (8) Concentrations of polypetides analogous to human ApoC, ApoD and "arginine-rich" polypeptide, if present, were too low for their unequivocal chemical characterization.
Atherosclerosis
PMID:Lipid transport in the avian species. Part I. Isolation and characterization of apolipoproteins and major lipoprotein density classes of male turkey serum. 18 83

The content and percent composition of cholesterol, triglyceride, phospholipids, and total proteins in HDL-2 and HDL-3 were quantitated in 5 women with familial hyperalphalipoproteinemia to determine if there are any distinctive characteristics of the high density lipoproteins in this heritable disorder. The 5 women with familial hyperalphalipoproteinemia (FHA) were compared to 4 normal women, with the groups being comparable in regards to age (40 +/- 3 and 37 +/- 5 years), total plasma cholesterol (202 +/- 9 and 188 +/- 16 mg/100 ml), triglyceride (75 +/- 12 and 95 +/- 19), and differing in levels of high density lipoprotein cholesterol (C-HDL, 84 +/- 6 and 61 +/- 3 mg/100 ml) respectively. Total cholesterol in the HDL-2 and HDL-3 fractions obtained by ultracentrifugation were 43.2 +/- 3.3 and 33.8 +/- 4.1 in FHA subjects, higher than total cholesterol in HDL-2 and HDL-3 in normals, 25.8 +/- 6.2 and 21.5 +/- 1.3 mg/100 ml, P less than 0.025. Total concentration of HDL-3 was higher in FHA than in normal subjects, respectively 222.4 +/- 22.6 and 149 +/- 7.2 mg/100 ml, P less than 0.025. Lipid-protein percent composition of HDL-2 and HDL-3 in FHA and normals was nearly identical, and polyacrylamide gel electrophoresis revealed no qualitative differences in band migration and appearance of the HDL-2 and HDL-3 fractions in normal and FHA subjects. In these women with FHA, there appears to be an increased concentration of normal HDL-2 and HDL-3.
Atherosclerosis 1976 Oct
PMID:Composition of HDL-2 and HDL-3 in familial hyperalphalipoproteinemia. 18 77

In epididymal adipose tissue from rats, human serum antagonizes inhibition of basal lipolysis by nicotinic acid in vitro. Under similar conditions caffeine-stimulated lipolysis was unaffected by the presence of human serum. Very low density (VLDL), low density (LDL) and high density (HDL) lipoproteins were all found to antagonize the action of nicotinic acid on basal lipolysis. VLDL also antagonized prostaglandin E1 (PGE1)-inhibition of basal lipolysis in vitro. The fat cell membrane was suggested as the site at which human serum lipoproteins antagonize nicotinic acid or PGE1 antilipolytic action on basal lipolysis in vitro.
Atherosclerosis 1976 Oct
PMID:Modification of nicotinic acid and prostaglandin E1 antilipolytic action in vitro. 18 78


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