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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human aortic endothelial cells, isolated at autopsy from a 52-year-old male dying from lung cancer, were treated with simian virus 40 (SV40). One colony was isolated from the infected endothelial cell culture 4 weeks after infection. The cells expressed SV40 large T antigen and p53 protein (p53) in their nuclei but lacted the characteristics of a transformed phenotype. The cells grew well in a monolayer over the 97th passage and exhibited Factor VIII-related antigen, Ulex europaeus 1 agglutinin (UEA-1) as endothelial cell markers, and a well-developed fibronectin network. The amount of prostacyclin synthesized by the cells was less than the amount synthesized by normal aortic or umbilical cord vein endothelial cells. The cells produced relatively large amounts of procollagenase, and 12-o-tetradecanoyl-phorbol-13-acetate (TPA) augmented the ability of the cells to produce this enzyme. These immortalized human aortic endothelial cells, which have some characteristics of normal endothelial cells and, like capillary endothelial cells, have the ability to produce collagenase, will probably prove useful for studies of atherosclerosis and angiogenesis.
Virchows Arch B Cell Pathol Incl Mol Pathol 1991
PMID:Collagenase production by immortalized human aortic endothelial cells infected with simian virus 40. 167 13

Present knowledge in the field of vascular endothelial cells is reviewed. The role of endothelial cells in the synthesis of matrix proteins and glycosaminoglycans is described. Endothelial cells play a considerable role in the processes of coagulation and fibrinolysis. They also interact with neurotransmitters and vasomotoric substances, and participate in inflammation and immunological responses. They produce several different growth factors. Their role in lipoprotein metabolism is of special importance to research into atherosclerosis.
Virchows Arch B Cell Pathol Incl Mol Pathol 1991
PMID:Biochemical properties of vascular endothelial cells. 168 34

Corpulent male rats of the atherosclerosis prone JCR:LA-corpulent strain were fed diets supplemented with 10% by weight of olive oil or red fish oil. These rats are obese, with VLDL hyperlipidemia and marked insulin resistance. The diets were maintained to 9 months of age. Olive oil-fed rats had a 45% reduction in triglyceride concentrations with no significant changes in cholesterol or phospholipids. Red fish oil caused significant reduction in all lipid classes, with a 65% reduction in triglycerides and 35% reduction in cholesterol concentrations. Olive oil caused increases in the relative concentrations of oleic acid-containing triglycerides, while red fish oil preferentially enriched the longer chain fatty acids. There were no significant changes in insulin or glucose metabolism. The incidence of myocardial lesions, characteristic of the JCR:LA-cp strain, was unaltered by either oil-supplemented diet. These results, in a spontaneous animal model for cardiovascular disease, are consistent with other studies showing that diets rich in n-3 fatty acids do not, in themselves, confer protection against cardiovascular disease in animal models with genetically or experimentally induced lipid disorders.
Exp Mol Pathol 1991 Dec
PMID:Effect of dietary n-3 fatty acids on atherosclerosis prone JCR:LA-corpulent rats. 174 17

One of the hypotheses trying to explain the process of aging is the idea of glycation of proteins. This reaction, also called the Maillard or browning reaction, may explain age-related symptoms such as cataract, atherosclerosis and modification of collagen-containing tissues. Diabetics, which possess elevated blood sugar levels, show signs of accelerated aging exposing similar complications. The Maillard reaction, which occurs on a large scale in vivo, may play a key role in the initiation of these symptoms.
Mol Biol Rep 1991 May
PMID:The role of glycation in aging and diabetes mellitus. 174 74

Cholesterol oxidase (3 beta-hydroxy-steroid oxidase) catalyzes the oxidation of cholesterol to 4-cholesten-3 one and other oxidized cholesterol derivatives. The purpose of the present study was to investigate its effects on cultured vascular smooth muscle cells. Cultured rabbit aortic smooth muscle cells were morphologically altered after exposure to cholesterol oxidase in the presence of culture medium containing 10% fetal calf serum. If fetal calf serum was absent, cells were unaffected by the treatment. The extent of morphological change of the smooth muscle cells was dependent upon the time of exposure to the enzyme and the concentration of cholesterol oxidase employed. After moderate treatment with cholesterol oxidase, cells excluded trypan blue. Further, a specific mitochondrial marker DASPMI (dimethyl aminostyryl-methyl-pyridiniumiodine) which was used as a fluorescent index of cell viability, revealed that cell viability was unchanged after moderate cholesterol oxidase treatment. Nile red, a hydrophobic probe which selectively stains intracellular lipid droplets, was applied to detect the cellular lipid content after treatment with cholesterol oxidase. Cellular nile red fluorescence intensity increased linearly with the time and concentration of cholesterol oxidase treatment. These results demonstrate that cholesterol oxidase alters lipid deposition in the cell and changes cell morphology. The primary site of action of cholesterol oxidase appears to be independent of the cell membrane itself and instead is dependent upon the lipid content in the surrounding culture media. These changes occur prior to the cytotoxic effects of extensive oxidation. Because oxidized cholesterol may play an important role in the pathogenesis of atherosclerosis, our results have implications for intracellular accumulation of lipids in smooth muscle cells during the atherosclerotic lesion.
Mol Cell Biochem 1991 Nov 13
PMID:Effects of cholesterol oxidase on cultured vascular smooth muscle cells. 177 Sep 44

It has been proposed that low density lipoprotein (LDL) must undergo oxidative modification before it can participate in atherosclerosis. The present paper studied the effect of cholesterol oxidation in LDL on cultured vascular smooth muscle cells. LDL was oxidized by cholesterol oxidase (3-beta-hydroxy-steroid oxidase) which catalyzes the oxidation of cholesterol to 4-cholesten-3 one and other oxidized cholesterol derivatives. Cholesterol oxidase treatment of LDL did not result in lipid peroxidation. Cultured rabbit aortic smooth muscle cells were morphologically changed following exposure to cholesterol oxidized LDL. Nile red, a hydrophobic probe which can selectively stain intracellular lipid droplets, was applied to detect the cellular lipid content after treatment with oxidized or non-oxidized LDL cholesterol. LDL which did not undergo oxidation of its cholesterol had no effect on the cells. However, cellular nile red fluorescence intensity was increased as the pre-incubation time of cholesterol oxidase with LDL increased. This was supported by HPLC analysis which revealed that the oxidized cholesterol content of treated cells increased. These findings suggest that cholesterol oxidation of LDL can alter lipid deposition in the cells and change cell morphology. The oxidation of cholesterol in vivo may play an important role in the modification of LDL which could contribute to the generation of the lipid-laden foam cells.
Mol Cell Biochem 1991 Nov 13
PMID:Effects of oxidative modification of cholesterol in isolated low density lipoproteins on cultured smooth muscle cells. 177 Sep 45

Endothelial characteristics and the macrophage foam cell nature of early naturally occurring lesions in the aorta and coronaries of the pigeon have been well characterized. However, the characteristics of pigeon atherosclerosis at other vascular sites have not been extensively studied. The present study was designed to compare atherosclerosis in the brachiocephalic artery with that in the coronaries and aorta. Forty-six White Carneau (WC) pigeons (26 female, 20 male) ranging in age from 2.5 to 7 years were necropsied after fixation under deep anesthesia by perfusion at 160 mm Hg with buffered glutaraldehyde. Arteries stained with Sudan IV for gross evaluation were subsequently processed for SEM and TEM. The occurrence of sudanophilia in the proximal brachiocephalic artery was greater in females (22/26) than in male (2/20). The endothelium, as studied by SEM, was intact over all normal and sudanophilic areas. Cell morphology varied with location in the vessel and gradually changed from polygonally shaped cells with prominent margins and protruding nuclei in the proximal brachiocephalic artery to elongated, flattened cells in distal regions. These regional differences were consistently observed, and did not correlate with age, gender, or areas of lipid accumulation. Unlike lesions in the coronary arteries and at the celiac bifurcation of the aorta, a relative paucity of white blood cells over diffuse sudanophilic areas was observed. This lack of adherent monocytes correlated with lesion ultrastructure. Connective tissue in the intima of the sudanophilic brachiocephalic arteries was disorganized, reflecting both an increase in matrix components and the presence of massive pools of extracellular lipid. Intracellular lipid was minimal and when present was confined to random droplets in the cytoplasm of intimal smooth muscle cells. Monocyte-derived foam cells, characteristic to other vascular beds, were absent from the brachiocephalic artery lesions. These results document differential lesion composition in the WC pigeons and suggest a gender-related susceptibility for brachiocephalic artery atherosclerosis in pigeons.
Exp Mol Pathol 1991 Apr
PMID:Morphologic characteristics of naturally occurring atherosclerosis in the brachiocephalic artery of the pigeon. 202 38

Familial hypercholesterolemia is an inherited disease in humans that is caused by a deficiency in the receptor that mediates the internalization and degradation of low density lipoprotein. Patients that inherit two abnormal low density lipoprotein receptor alleles have severe hypercholesterolemia, advanced atherosclerosis, and life-threatening coronary artery disease that is refractory to conventional therapies. In this review, we discuss the prospects for gene therapy in the treatment of familial hypercholesterolemia.
Mol Biol Med 1990 Jun
PMID:Prospects for gene therapy of familial hypercholesterolemia. 221 9

The intracellular distribution of lipid shifts from cytoplasmic to lysosomal localization during the progression of atherosclerosis. It has been suggested that this shift may relate to regressability of lesions. The effects of reducing plasma cholesterol on the regression of early cholesterol-induced atherosclerosis were evaluated. Most small, early lesions disappeared after 5 weeks on the regression regimen. Larger lesions, however, did not change in extent even following 10 weeks regression. Although large lesions were not reduced in size under the regression conditions, total cytoplasmic lipid decreased. Paradoxically, the size of residual intracellular lipid deposits increased. The structural features of these remaining deposits suggest that they were lipid-filled lysosomes. Leukocyte adherence to endothelium, which increases 10- to 20-fold during progression, returned to control levels over most areas of large lesions. Levels of adherent leukocytes remained elevated, however, over small lesions and at the edges of larger lesions. Our data indicate that regression is not a uniform process, but rather, even in early lesions, varies within separate intimal microdomains. In addition, our data suggest that part of the difference may reside in differential partitioning of lipid into lysosomes.
Exp Mol Pathol 1990 Dec
PMID:Early atherogenesis in White Carneau pigeons: effect of a short-term regression diet. 225 30

We examined the correlation between elastolysis and abnormal accumulation of microfibrils in the arteries of rabbits using light and electron microscopic and tissue culture techniques. Partial constriction of the common carotid arteries of rabbits gave rise to gradual atrophy of the media with elastolysis and an unusual accumulation of microfibrils. With advancing experimental atherosclerosis in cholesterol-fed rabbits, the elastofibrotic intima generally became thick and hyalinized and was replaced by bundles of microfibrils lacking elastin or associated with only tiny elastin aggregates and disrupted elastic fibers. Organ cultures of aortic explants from rabbits with or without pancreatic elastase supplementation for 5 days disclosed that there was complete loss of medial elastic fibers and increasing deposition of microfibrils, morphologically identical to elastin-associated microfibrils, around viable smooth muscle cells only in the elastase supplemented group. These observations suggest that abnormal accumulation of microfibrils in the elastic tissue is closely associated with excessive elastolysis of preformed or newly formed elastic fibers during elastic tissue remodeling. Enhanced synthesis of microfibrils may occur in response to elastolysis as a reparative phenomenon.
Exp Mol Pathol 1990 Feb
PMID:Abnormal accumulation of elastin-associated microfibrils during elastolysis in the arterial wall. 230 10


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