Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
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Arterial intima proteins were extracted by 9 M urea from matching histologically atheroma-free areas of 27 human thoracic aortas of both sexes from younger (15-34) and older (35-82) age groups and studied after separation by high-resolution two-dimensional polyacrylamide gel electrophoresis. Seventeen specific protein groups on each gel were identified according to their relative charges and molecular weights and their distribution in the two age groups compared. Some plasma-derived proteins occurred rarely in young aortas while they were consistently found in those from older cases, i.e., protein group 4 (alpha 1-antichymotrypsin) 1/13 (8%) vs 12/14 (86%), group 7 (haptoglobin beta-chain) 1/13 (8%) vs 13/14 (93%) and groups 6 and 9 (IgG chains) 3/13 (23%) vs 9/14 (64%), respectively. Other plasma-derived proteins such as group 3 (albumin) and 5 (alpha 1-antitrypsin) were identified in all samples of both age groups but their expression in the aortic intima increased with age. Proteins which are typically found intracellularly such as those from groups 11 (actin), 12 (cytoskeleton proteins), and 13 (tropomyosin-like proteins) appeared in samples of intima of both age groups but were less apparent in older specimens. These studies suggest that the changes in aortic intima protein distribution in the absence of atherosclerosis closely correlate with histological changes such as intimal thickening often found with aging, providing new sensitive markers of vascular senescence.
Exp Mol Pathol 1985 Dec
PMID:Effect of aging on human aortic protein composition. II. Two-dimensional polyacrylamide gel electrophoretic analysis. 406 9

In spontaneously atherosclerosis-susceptible White Carneau pigeons intimal cushions are noted consistently at the coeliac branch of aorta at birth. While these cushions do not progress into atherosclerotic lesions, the area across from the cushion (so called "lesion area") develop a classic atherosclerotic plaque by three years of age. In order to explain this regional aortic susceptibility to atherosclerosis, cholesterol and cholesteryl ester concentrations and prostaglandin biosynthesis in the two aortic regions were examined. It was found that the concentration of free and esterified cholesterol was higher in the intimal cushion area. Examination of the formation of various prostaglandins from C14-arachidonic acid indicates a striking increase in PGE2 synthesis in the lesion area with no difference in the formation of 6-keto PGF1 alpha (stable product of PGI2). These studies suggest that one of the earliest changes noted in the "lesion area" that differs from the intimal cushion is the enhanced formation of PGE2.
Virchows Arch B Cell Pathol Incl Mol Pathol 1981
PMID:Regional aortic differences in atherosclerosis susceptibility. Relationship to lipid concentration and prostaglandin biosynthesis. 611 22

In spontaneously atherosclerosis-susceptible White Carneau pigeons, intimal cushions that appear at birth near the coeliac branch of aorta do not progress into atherosclerotic lesions. However, the area across from the intimal cushion (so called 'lesion area') a) accumulates cholesteryl esters b) synthesizes more PGE2 and c) eventually develops into complicated atherosclerotic plaques. When DOCA-salt hypertension is induced in the pigeons, the 'initimal cushion' area displays a) accumulation of increasing amounts of cholesteryl esters and b) increase in the synthesis of all prostaglandins (particularly PGE2) from C14-arachidonic acid and c) approaches similarity to the 'lesion area' in the magnitude of these changes. These results suggest that under the influence of a risk factor, the 'intimal cushion' can acquire biochemical properties of the atherogenic areas of the aorta.
Virchows Arch B Cell Pathol Incl Mol Pathol 1981
PMID:Regional aortic differences in atherosclerosis-susceptibility: changes in prostaglandin biosynthesis and cholesterol accumulation in response to desoxycorticosterone (DOCA)-salt induced hypertension. 611 75

Hypertension is a major risk factor for clinically significant atherosclerotic vascular disease in Western Society, although the link between these conditions remains very poorly understood. Recent studies which are reviewed here have demonstrated that major arterial intimal and medial abnormalities occur as a result of hypertension. These include functional changes in endothelial permeability as well as alterations in the endothelial cells themselves with an increase in their turnover and number and distinct changes in morphology. However, endothelial cell loss leading to denudation of the arterial intimal surface appears to be relatively uncommon. Intimal and medial thickening are consistent features of hypertension and result from increases in both cellular and extracellular components. The cells accumulating in the subendothelial space appear to be of both blood-borne and medial origins, although their complete characterization has not been performed as yet. The adherence of blood cells to the endothelial surface appears to be promoted by the presence of hypertension along with their increased entry into the intima through endothelial cell junctions. Medial thickening with hypertension is attributable primarily to increased smooth muscle cell mass, although enhanced deposition of collagen and elastin plays a contributory role. Recent data would indicate that smooth muscle cell hypertrophy rather than hyperplasia is primarily responsible for the greater smooth muscle mass with hypertension. Although elevated DNA content of hypertensive arteries has been demonstrated, such changes may be secondary to a marked increase in cells showing nuclear polyploidy. Prolonged normalization of blood pressure in hypertensive animals can produce considerable regression of arterial changes toward the control state. The changes appear more marked with respect to the cellular rather than the extracellular abnormalities induced by hypertension. In man, little is known about the effects of antihypertensive therapy on the vasculature itself, although clinical complications related to both hemorrhagic or thrombotic strokes are clearly reduced by blood pressure reduction. On the other hand, the influence of treatment on the atherosclerotic process or on the course of coronary artery disease and its complications is not currently understood. The accelerating effect of hypertension on atherosclerosis generally requires a critical level of circulating lipoproteins. Enhanced atherosclerosis is not observed in hypertensive animals without hyperlipoproteinemia or in human subjects with low lipoprotein concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)
Exp Mol Pathol 1984 Aug
PMID:Recent advances in molecular pathology. The effects of hypertension on the arterial wall. 638 Oct 89

The term human serum high density lipoprotein (HDL) represents a range of lipid-protein complexes which are identified by their density and hence their relative lipid-protein content. Because HDL composition is variable, any proposed mechanisms for lipid and protein exchange must account for this variability. More importantly, since HDL has been repeatedly shown to be a negative risk factor in atherosclerosis, physical interactions have to be put in a physiological context. In this review, the lipid and protein exchange reactions of HDL with other lipoproteins, phospholipid vesicles, lipid-coated glass beads and isolated cells, will be considered. Particular emphasis will be placed on the role of the two major apoproteins of HDL, namely apo A-I and apo A-II, in these exchange reactions and a model will be presented to explain how these apoproteins might mediate lipid exchange, interconversions of lipoprotein particles, and the egress and excretion of lipid from cells.
Mol Cell Biochem 1983
PMID:High density lipoprotein exchange reactions. 641 Jan 79

Young adult male rhesus monkeys (Macaca mulatta) were fed an atherogenic diet for 38 months. After 38 months of atherosclerosis induction, a baseline group was selected and necropsied to determine the extent and severity of atherosclerosis before regression regimens were begun. The remaining animals were fed diets that varied in cholesterol concentration in order to maintain plasma cholesterol concentrations of approximately 200 or 300 mg/dl for either 24 or 48 months. The progression or regression of atherosclerosis in coronary arteries, abdominal aorta, and carotid arteries was determined by comparing them to the baseline group. Coronary artery atherosclerosis regressed in the majority of animals after 4 years but not after 2 years when plasma cholesterol concentrations were about 200 mg/dl. Among the animals maintained at plasma cholesterol concentrations of about 300 mg/dl, about half the animals progressed in the extent of coronary artery atherosclerosis while about half regressed. The majority of the animals that progressed in lesion extent were genetic hyperresponders to dietary cholesterol whereas those that regressed were predominantly hyporesponders, even though their plasma lipid concentrations were equivalent during the regression phase. The changes seen in atherosclerosis extent in the abdominal aorta were quite similar to the changes seen in coronary arteries. Changes at this site were not pronounced after 2 years, but after 4 years animals with plasma cholesterol concentrations of about 300 mg/dl progressed while the animals at 200 mg/dl were mostly unchanged. No evidence for atherosclerosis regression was found in the common carotid arteries or in the carotid bifurcations.
Exp Mol Pathol 1984 Aug
PMID:A study of atherosclerosis regression in Macaca mulatta. V. Changes in abdominal aorta and carotid and coronary arteries from animals with atherosclerosis induced for 38 months and then regressed for 24 or 48 months at plasma cholesterol concentrations of 300 or 200 mg/dl. 646 38

The abdominal aortas of five groups of young male Yorkshire swine were studied: (1) 0-day baseline group; (2) hyperlipidemic (HL) group with ballooning; (3) mash group with ballooning; (4) mash group without ballooning; and (5) HL group without ballooning. The last four groups were injected with [3H]thymidine at 270 days and sacrificed subsequently in subsets at intervals up to 75 days in order to study births and deaths (or loss by migration) among cells over the period 270-345 days. However, only in the HL-ballooned group were there enough swine for the isotopic data to be useful for most purposes. In the 0-day baseline group there were 6 +/- 2 X 10(6) cells in intimal cell masses (ICM); in the 270- to 345-day mash group without ballooning the number was 10 +/- 2 X 10(6), which is not a statistically significant increase over 0-day. This supports the hypothesis that in the normal state births and deaths (or loss by migration) among cells in ICM are nearly balanced at least up to 1 year of age. In the 270- to 345-day mash group with ballooning there were 61 +/- 12 X 10(6) cells in the ICM. Thus a single episode of deendothelialization results in tremendous hyperplasia of ICM. However, even the largest ICM (atherosclerotic lesion) in this group showed essentially no necrosis. In the 270- to 345-day HL group with ballooning there were 108 +/- 17 X 10(6) cells in the ICM turned atherosclerotic lesions. In addition an average of one-third of the lesion volume was occupied by lipid-rich, calcific necrotic debris. Thus the HL diet appears to have associated with it both mitogenic and cytotoxic influences on ICM cells. In the 270- to 345-day HL group not ballooned there were 130 +/- 30 X 10(6) lesion cells and lesions were somewhat more extensive and necrotic than in the HL-ballooned group, probably because the former group included by chance more hyperresponders (as regards serum cholesterol values) to the HL diet than the latter. Regardless of this, the data suggest that in this particular model of advanced atherosclerosis the balloon-injury stimulus to proliferation and the HL-diet stimulus are neither additive nor synergistic.(ABSTRACT TRUNCATED AT 400 WORDS)
Exp Mol Pathol 1983 Dec
PMID:Population dynamics of arterial cells during atherogenesis. XIII. Mitogenic and cytotoxic effects of a hyperlipidemic (HL) diet on cells in advanced lesions in the abdominal aortas of swine fed an HL diet for 270-345 days. 664 17

Punch-biopsy specimens were obtained from uninvolved areas of the proximal aorta of each of 60 patients with atherosclerosis undergoing cardiovascular surgery. Electron microscopic study of the smooth muscle and endothelial cells of the aortas showed cellular hyperplasia, nuclear and nucleolar atypia. Virions of the Herpesviridae family were observed in ten of the patients. They were detected in occasional smooth muscle and rare endothelial cells. Specimens were taken from three separate sites of each aorta and distributed into five blocks for each patient. In only a single block from each of the ten positive patients could virus be identified. Nine of the ten virus-positive patients also exhibited intracytoplasmic microtubular inclusions. In four patients only the microtubular inclusions were seen. Microcapillaries were observed in the midportion of the media, which we consider to be an attempt of a repair process.
Exp Mol Pathol 1984 Jun
PMID:Herpesviridae in the endothelial and smooth muscle cells of the proximal aorta in arteriosclerotic patients. 672 37

Hybrid hares provide a model for induction of aortic atherosclerosis. The basic dietary regimen consisted of cholesterol-supplemented and nonsupplemented commercial pellets alternating at 1-week intervals for up to 18 months. Controls were fed nonsupplemented pellets. Control aorta features included branch cushions, intimal thickenings unrelated to branches, and several longitudinal layers of smooth muscle in the outer media. Branch cushions extended longitudinally in the main vessel, and had multidirectional, streamlike bundles of smooth muscle in the intima and media. Intimal thickenings unrelated to branches occurred as longitudinal patches, most frequently in the ventral quadrant. The adjacent media had a regular array of cells. Raised lesions concentrated at branch orifices and in the ventral quadrant. Lesions involved up to 80% of the thoracic and 40% of the abdominal aorta by 5 months. Predominant lesions consisted of superficial fibromuscular tissue and deeper foam cells and stainable lipids. Some of these lesions were atheromata with fibrous cap. Fibromuscular plaques, 120 to 150 micron thick, had a few superficial foam cells and hydropic degeneration. Foam-cell lesions were also observed. Data obtained suggest the importance of branch cushions and intimal thickenings unrelated to branches, and of the periods on nonsupplemented pellets.
Exp Mol Pathol 1983 Aug
PMID:Mosaicism in female hybrid hares heterozygous for glucose-6-phosphate dehydrogenase. IV. Aortic atherosclerosis in hybrid hares fed alternating cholesterol-supplemented and nonsupplemented diets. 687 51

The phase states and phase transitions of some lipids, lipid mixtures of blood and tissues of some animals and human were examined by the method of scanning calorimetry (DSC-2, "Perkin--Elmer"). It was determined that in monohydrated and in hydrated systems, cholesterol produces a liquefying effect on the total phospholipids of the brain and blood. In complex multicomponent lipid systems changes of the phase states and of temperatures of the phase transitions of some lipids were discovered. The role of these phase transitions and miscibility of lipids for functioning of the cellular membranes and of the key-enzymes in the process of changes of lipoproteins of the blood (LCAT) is being discussed, as well as the connection of the phase transitions of cholesterol esters of the blood with atherosclerosis.
Mol Biol (Mosk)
PMID:[Phase transitions, lipid-lipid interactions and their role in some biostructures]. 732 25


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