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V S Repin

Publications and source records attributed to V S Repin.

At least 37 records · Page 2Linked to original sources
PubMed1990

Inhibition of cholesterol synthesis and esterification regulates high density lipoprotein interaction with isolated epithelial cells of human small intestine.

The effect of two inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, lovastatin and monacolin L, and an inhibitor of acyl coenzyme A:cholesterol acyltransferase (ACAT), Sandoz compound 58-035, on the interaction of 125I-labeled high density lipoprotein-3 (HDL3) with isolated human enterocytes was studied. Both HMG-CoA reductase inhibitors inhibited cholesterol synthesis and 125I-labeled HDL3 binding and degradation by enterocytes; a strong correlation between changes in cholesterol synthesis and interaction of 125I-labeled HDL3 with cells was observed. Lovastatin caused reduction of the apparent number of 125I-labeled HDL3 binding sites without affecting the binding affinity. No changes of cell cholesterol content were observed after incubation of cells with lovastatin. Mevalonic acid reversed the effect of lovastatin on 125I-labeled HDL3 binding. Lovastatin blocked up-regulation of the HDL receptor in response to loading of cells with nonlipoprotein cholesterol and modified cholesterol-induced changes of 125I-labeled HDL3 degradation. Lovastatin also reduced HDL-mediated efflux of endogenously synthesized cholesterol from enterocytes. The ACAT inhibitor caused a modest increase of 125I-labeled HDL3 binding to enterocytes and significantly decreased its degradation; both effects correlated with inhibition of cholesteryl ester synthesis. The results allow us to assume that the intracellular free cholesterol pool may play a key role in regulation of the HDL receptor.

Anticholesteremic Agents↗
PubMed1990

[Study of HDL2-dependent synthesis of bile acids in culture of rabbit hepatocytes: effects of oxidized cholesterol derivatives].

The effect of individual oxysterols--products of auto-oxidation of cholesterol on bile acid synthesis by cultivated rabbit hepatocytes was studied. Relative rates of bile acid synthesis were measured as the conversion of 4-14C cholesterol-HDL2 into total 4-14C labeled bile acids. 7 beta-hydroxycholesterol and 3,5-cholestane-7-dione strongly inhibited bile acid synthesis at concentrations 1-10 micrograms/ml. These data support the hypothesis that oxidized cholesterol derivatives accelerate the development of hypercholesterolemia in rabbits fed on cholesterol containing diet.

Animals↗
PubMed1990

[Agonist-induced platelet adhesion: use of the method in patients with myocardial infarction].

A new method of agonist-induced platelet adhesion has been developed for the evaluation of platelet activity. Platelet adhesion to plastic was stimulated by low doses of ADP, epinephrine and stable thromboxane analogue U46619. These inducers cause more than 3-fold increase of platelet adhesion in concentrations by 5-10 times lower than those necessary for stimulation of platelet aggregation in Born aggregometer. The method was applied for evaluation of platelet adhesive activity in patients with myocardial infarction. A dramatic increase of agonists-induced platelet adhesion was registered in patients with acute infarction, most significantly expressed when epinephrine was used as platelet agonist.

Adenosine Diphosphate↗
PubMed1990

[The effect of khellin and timefurone on secretion and catabolism of lipoproteins by cultured human and rabbit hepatocytes].

Using human and rabbit hepatocyte cultures, the effects of khellin and timefurone on lipoprotein metabolism were studied with special reference to the following parameters: i) binding and degradation of 125I-labeled low density lipoproteins (LDL); ii) apoprotein B (apo-B) secretion measured by immunoenzymatic assay, iii) [35S]methionine labeled apo-B and apo-E within the composition of very low density lipoproteins (VLDL); iiii) total cholesterol synthesis and cholesterol secretion within the composition of VLDL. The therapeutic concentrations (0.1-10 micrograms/ml) of the above drugs had no appreciable effect on the binding and degradation of 125I-LDL but inhibited the secretion of apo-B VLDL, leaving the apo-E VLDL unaffected. This was paralleled with inhibition of cholesterol synthesis (by 30-50%) and VLDL secretion. These results suggest that khellin and timefurone mediate the hypolipidemic effect via the reduction of the intracellular synthesis of cholesterol and secretion of apo-B containing VLDL by hepatocytes.

Animals↗
PubMed1990

[Stimulation of cholesterol ester synthesis in macrophages by lipoproteins from normal and atherosclerotic human aorta intima].

A buffer extract from homogenized human aorta was applied to a Bio-Gel A-15m column, and two cholesterol-containing peaks were resolved. Both fractions of aortic lipoproteins present in the extracts from normal and atherosclerotic intima and stimulated cholesteryl ester (CE) synthesis in J774 mouse macrophages caused unregulated loading with CE. The Vmax of CE formation in the presence of both fractions correlated with the degree of intimal atherosclerosis. An excess of both fractions did not inhibit the uptake of malondialdehyde-treated low density lipoproteins by macrophages; their interaction with the cells was not inhibited either by fucoidin or by dextran sulfate. The uptake of labeled LDL by human fibroblasts was markedly decreased with excess of both fractions. Aortic lipoprotein-mediated CE synthesis (for both fractions) was completely blocked by EDTA in fibroblasts, being decreased by 50% in macrophages.

Animals↗
PubMed1989

Effect of cell cholesterol content on apolipoprotein B secretion and LDL receptor activity in the human hepatoma cell line, HepG2.

Human hepatoma HepG2 cells were used to study the effects of cholesterol loading and depletion on apolipoprotein B (apoB) secretion and low-density lipoprotein (LDL) receptor activity. Exposure of HepG2 cells to cholesterol and oleic acid, which elevated intracellular cholesterol levels, stimulated apoB secretion and reduced receptor-mediated uptake of LDL, whereas recombinant complexes of apolipoprotein A-I with dimyristoylphosphatidylcholine, which depleted the cellular cholesterol pool, inhibited apoB secretion and up-regulated LDL receptors. Significant negative correlation (r = -0.92, P less than 0.001) between the levels of apoB secretion and LDL uptake was found. These data suggest that the cholesterol content of the cells may induce concomitant changes in apoB secretion and LDL receptor activity.

Apolipoprotein A-I↗
PubMed1989

Binding and uptake of native and modified low-density lipoproteins by human hepatocytes in primary culture.

The binding and uptake of native low-density lipoproteins and malondialdehyde-treated low density lipoproteins by human hepatocytes in primary culture has been analyzed. Experiments with 125I-labeled malondialdehyde-treated low-density lipoproteins showed that cultured liver cells took up and degraded malondialdehyde-treated low-density lipoproteins, but the cell type(s) responsible for this action remain unclear. Immunofluorescent visualization of receptor-bound low-density lipoproteins revealed that low-density lipoprotein binding sites were distributed on the surface of nearly all cells of the culture. Binding sites for malondialdehyde-treated low-density lipoproteins were found in only 5% of the cultured cells, and these cells differed from hepatocytes in shape and size. Cultured hepatocytes internalized and native low-density lipoproteins, but not malondialdehyde-treated low-density lipoproteins, labeled with the fluorescent dye 3',3'-dioctadecylindocarbocyanine. About 15% of the cells that take up 3',3'-dioctadecylindocarbocyanine-labeled malondialdehyde-treated low-density lipoproteins could be identified as liver endothelial cells and macrophages, since they internalized formaldehyde-treated human albumin and fluorescent carboxylated microspheres. Our results indicate that human hepatocytes in primary culture express surface receptors for native low-density lipoproteins but not for modified low-density lipoproteins.

Cells, Cultured↗
PubMed1989

Very low density lipoprotein secretion by cultured hepatocytes of rabbits fed purified or autoxidized cholesterol.

The main objectives of this study were to compare the effects of dietary commercial cholesterol (containing 5% of oxidized cholesterol derivatives) and purified cholesterol on the secretion rate of very low density lipoprotein apolipoproteins and lipids by cultured rabbit hepatocytes and to verify the hypothesis that products of cholesterol autoxidation stimulate the rapid development of hypercholesterolemia. Rabbits fed dietary (old) commercial cholesterol for six weeks showed a fivefold increase in the serum concentration of cholesterol compared with that in purified cholesterol-fed rabbits. The secretion rates of very low density lipoprotein total protein and very low density lipoprotein [3H]apolipoproteins were similar for the hepatocytes of these two cholesterol-fed groups of animals and were two- and threefold greater, respectively, than for cells from control rabbits. Cholesteryl ester content of the hepatocytes from dietary (old) commercial cholesterol-fed rabbits was dramatically increased in comparison with hepatocytes from control and purified cholesterol-fed rabbits. The elevated intracellular cholesteryl ester content is assumed to account for such an increase of very low density lipoprotein-cholesteryl ester secretion by cells prepared from dietary (old) commercial cholesterol-fed rabbits. These effects appear to be caused by activation of cholesterol esterification by oxidized cholesterol derivatives. The rapid development of hypercholesterolemia induced by dietary (old) commercial cholesterol is associated, at least in part, with the stimulated production of hepatic very low density lipoprotein apolipoproteins and cholesteryl esters.

Animals↗
PubMed1989

Noradrenaline induces the polyploidization of smooth muscle cells: the synergism of second messengers.

The effect of noradrenaline (NA) on DNA replication of cultured smooth muscle cells (SMC) isolated from rat aorta was examined. It was found that 10 microM NA significantly increased (approximately by twofold) the frequency of tetraploid cells. Cultivation of 4C cells isolated by flow cytometric cell sorting revealed that they were true polyploid cells. This receptor-mediated effect of NA was blocked only by simultaneous action of alpha- and beta-adrenoreceptor antagonists. SMC polyploidization was also stimulated by simultaneous application of direct activators of "second messenger" systems forskolin and phorbolmyristate-acetate. Thus, NA may be one of mediators of the "hypertensive" response of vessel wall SMC, which probably occurs due to synergism of two second messenger systems.

Animals↗
PubMed1989

Synergistic potentiation of polyphosphoinositide breakdown by adenylate cyclase coupled receptors in human endothelial cells.

Histamine induces dose-dependent increases in inositol-monophosphate, inositol-bisphosphate, and inositol-triphosphate in cultured human pulmonary artery and umbilical vein endothelial cells. Preincubation with isoproterenol results in synergistic potentiation of polyphosphoinositide breakdown. Isoproterenol does not change the effect of histamine, however, it does increase the potency of histamine in stimulating phosphoinositide turnover. This effect of isoproterenol is time-dependent reaching 350% at 120 min of preincubation. A synergistic potentiation of histamine-induced polyphosphoinositide breakdown by cyclic AMP stimulators has been observed after pretreatment of cultured endothelial cells with forskolin, dibutyryl cyclic AMP and cholera toxin. Our data suggest that isoproterenol potentiates histamine-induced polyphosphoinositide breakdown by operating via the adenylate cyclase system. This is the first evidence of synergistic potentiation of polyphosphoinositide breakdown by adenylate cyclase-coupled receptors in cultured human endothial cells.

Adenylyl Cyclases↗
PubMed1989

Platelet interaction with [125I]-labeled collagen type III: requirement of fibrillar structure formation.

Interaction of collagen type III (CIII) with washed human platelets was studied using CIII preparation from human placenta. CIII was labeled with [125I] and [125I]-CIII in monomeric and fibrillar form [( 125I]-CIIIm and [125I]-CIIIf respectively) were incubated with platelets at room temperature. Platelet-associated and free labels were separated by centrifugation through 20% sucrose. Binding of [125I]-CIIIf was unsaturable, linearly dependent on the concentration of label and represented 28 +/- 3% of the added protein. In comparison with CIIIf, binding of [125I]-CIIIm was minimal and represents only 0.9 +/- 0.2% of the added protein. The binding of [125]-CIIIm was also nonsaturable and linearly depend on the concentration of the labeled protein. Platelet activation neither increases the CIIIf binding, nor stimulates the binding of CIIIm. The binding of [125I]-CIIIf was not inhibited by the excess of the unlabeled CIIIm. The data obtained suggests the absence of high-affinity collagen receptors in platelets and corroborates the hypothesis of multiple low-affinity interactions between collagen fibrils and platelet surface. Binding of CIIIf was very fast--the level of binding reached a plateau within 1 min, and was similar in the presence of Ca2+/Mg2+ and EDTA. Spectrophotometrically undetectable microfibril formation during the lag phase of fibrillogenesis was sufficient for nearly the same as with large fibrils binding of CIII to platelets. Unlike platelets red blood cells (RBC) fail to bind significant amounts of [125I]-CIIIf.

Autoradiography↗
PubMed1989

Effect of plasmapheresis on the liver uptake of ApoB-lipoproteins labeled with technetium-99m.

To study liver low density lipoprotein (LDL)-receptor activity before and after plasmapheresis, [99mTc] very low density lipoprotein (VLDL) was used. Autologous VLDL was labeled, sterilized by filtration, and administered intravenously to patients under a gamma camera. The uptake of lipoproteins in the liver was measured by scintiscanning. Liver activity curves were generated for each patient. The liver activity in patients with the heterozygous form of familial hypercholesterolemia (FH) and in patients with symptomatic atherosclerosis (SA) without hereditary deficit of LDL receptors was reduced as compared to healthy people. Plasmapheresis enhanced the liver uptake of the 99mTc-labeled lipoproteins in atherosclerotic patients. Thus, labeled metabolites could presumably be of use in assessing the effect of plasmapheresis on liver function.

Adult↗
PubMed1989

[Determination of antithrombocyte antibodies in the blood serum of patients with idiopathic thrombocytopenic purpura by an immunoenzyme method].

Enzyme-linked immunosorbent assay (ELISA) was developed for determination of serum antiplatelet antibodies. Platelets obtained from healthy donors of blood group 0(1) were washed off plasma and sedimented on the bottom of microtest wells. After washing off unattached platelets and blocking of plastic with albumin platelets were incubated with sera under investigation and binding of serum antibodies was detected using antihuman immunoglobulin antibodies conjugated with peroxidase. Ten patients with idiopathic thrombocytopenic purpura (ITP). 1 patient with systemic lupus erythematosus. 1 patient with red blood cell aplasia and 9 healthy donors (negative control) were studied by ELISA. Serum antibodies which effectively bound to platelets were detected in 5 patients with ITP, in patient with lupus erythematosus and in patient with red blood cell aplasia.

ABO Blood-Group System↗
PubMed1989

[The effect of temperature and Ca2+ on the interaction of high-density lipoproteins with epithelial cells in the human small intestine].

The effect of temperature and Ca2+ ions on the interaction of high-density lipoprotein (HDL3) with human enterocytes was studied. It was shown that Kd measured at 4 degrees C is similar to that at 37 degrees C. Maximal number of binding sites at 37 degrees C is 15-fold times higher than that at 4 degrees C. EDTA (10 mM) and CaCl2 (0.5-5 mM) did not affect binding and uptake of HDL3 by human enterocytes. The obtained results indicate that HDL3-binding with these cells depends on temperature and does not depend on Ca2+ ions.

Adolescent↗
PubMed1989

[Characteristics of the interaction of blood monocytes with the arterial intima in swine exposed to catecholamines].

Adhesion and transendothelial migration of autologous blood monocytes have been studied in perfused swine arteries before and after injury produced by catecholamines. It has been shown that in the absence of plasma chemoattractant factors the damage of the vessel wall provides a significant increase in the number of monocytes adhered to the intima or migrated into intimal layer. The proportion of monocytes in these areas becomes 5 folds higher than in control regions. Possible immunological and not immunological mechanisms of mononuclear cells infiltration of the arterial intima are discussed.

Animals↗
PubMed1989

[Secretion of very low density lipoproteins by cultured rabbit hepatocytes with hypercholesteremia, induced by purified cholesterol and containing autooxidation products].

To evaluate the impact of oxidized derivatives of cholesterol on the development of hypercholesterolemia in rabbits, the secretion of very low density lipoprotein (VLDL) apoproteins and lipids was studied in cultures of hepatocytes obtained from: i) control rabbits, ii) rabbits fed on purified cholesterol (PCH), and, iii) rabbits fed on old commercial cholesterol (OCH) containing 5% of oxidized cholesterol derivatives. The rabbits fed on OCH for 6 weeks revealed a 5-fold increase in the serum cholesterol level compared with that in PCH-fed rabbits. The secretion of VLDL apoproteins and lipids by hepatocytes of two cholesterol-fed groups was similar, but was 2-3 times as high as that of cells from control rabbits. The cholesterol ester content in hepatocytes and the secretion of VLDL cholesterol esters by hepatocytes from OCH-fed rabbits was dramatically increased in comparison with hepatocytes from control and PCH-fed rabbits. These effects appear to be caused by the activation of cholesterol esterification by oxidized cholesterol derivatives. The rapid development of hypercholesterolemia in OCH-fed rabbits is at least partly associated with the stimulation of hepatic VLDL production.

Animals↗
PubMed1989

[Apoprotein B: its plasma level and interaction with cultured fibroblasts].

To study the relationship between the ability of apolipoprotein B (apo B) to interact with LDL receptors and its blood concentration, enzyme immunoassay was used to measure serum apo B levels in 51 healthy donors, 84 patients with coronary heart disease (CHD), and 22 newborns. Employing the same serum samples, the binding of apo B to fibroblasts was determined by the enzyme immunoassay modified for cultured cells. The mean values of apo B concentrations were found to be 0.89 +/- 0.25 mg/ml in the donors, 1.29 +/- 0.51 mg/ml in CHD patients, and 0.57 +/- 0.19 mg/ml in the newborns, while the apo B binding to the cells amounted to 108.9 +/- 16.7, 141.5 +/- 43.6, and 55.0 +/- 24.6 ng/mg, respectively. The mean values of serum apo B binding in the healthy donors and CHD patients were shown to correspond to the concentration relationship of pure LDL interaction with LDL receptors. The findings suggest that higher plasma apo B concentrations in CHD patients cannot be explained by lowered ability of serum apolipoproteins B to interact with LDL receptors of the cells.

Adult↗