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V S Repin

Publications and source records attributed to V S Repin.

At least 91 records · Page 5Linked to original sources
PubMed1988

Interconversions of HDL subfractions in normolipidemic and hypoalphacholesterolemic sera incubated with fibroblasts and hepatoma cell line Hep-G2.

Gradient gel electrophoresis was used to study the changes in the HDL subfractional spectrum according to the particle size during their interaction with hepatoma Hep-G2 cells and human skin fibroblasts. Incubation of normolipidemic sera with Ch-loaded fibroblasts resulted in a drop in small particle (HDL3a' HDL3b, HDL3c) and, a rise in large particle (HDL2b, HDL2a) proportions. In contrast, incubation of the same sera with hepatoma cells caused a decrease in HDL2b proportion and a HDL3a release. Incubation of hypoalphacholesterolemic sera with fibroblasts showed a decrease in HDL3b, HDL3c particles and an increase only in HDL2a. The proportion of HDL2b rose considerably when the sera were incubated with hepatoma cells. It is concluded that not only low HDL sera levels, but also the formation of defective HDL2b particles which interact less effectively with liver cells, are characteristic of hypoalphacholesterolemia.

Adult↗
PubMed1988

[An immunoenzyme method of diagnosing familial hypercholesterolemia].

A new modification of enzyme immunoassay: enzyme-linked-immunoreceptor assay (ELIRA)--was used to study the activity of LDL-receptors on cultured fibroblasts from 10 patients with elevated plasma cholesterol levels, IHD, accelerated atherosclerosis and xanthomatosis. Four patients were found to have heterozygous form of familial hypercholesterolemia. We have also shown that the results of ELIRA were quantitatively similar to the data obtained by traditional radioisotopic method. This indicates that simple, rapid, inexpensive ELIRA can be used for diagnosis of FH.

Cell Membrane↗
PubMed1988

[Potentiation of damaging effects of angiotensin II on the endothelium of the rabbit aorta by a beta adrenergic receptor agonist, isoproterenol].

Beta-adrenoceptor agonist isoproterenol potentiates the damaging effect of angiotensin II on rabbit aorta endothelium. Compared to the action of angiotensin II alone the amounts of injured cells, damaged intercellular contacts, cell form change, silver uptake and 125I--LDL uptake are increased under simultaneous action of angiotensin II and isoproterenol. Disturbance in barrier function is associated with the damaged cell contracts and cell death. 125I--LDL uptake increase is due to their accumulation in the adventitia. The simultaneous increase in angiotensin II and beta-adrenoceptor activating agents concentrations can damage endothelium and disturb its barrier function.

Angiotensin II↗
PubMed1988

[Detection of fibronectin and collagen types I, III, IV and V in semithin sections of the human aorta].

Localization of fibronectin and types I, III, IV and V collagen was investigated in semithin sections of fibrous atherosclerotic plaques and apparently normal intima of human aorta. The effect of different techniques of fixation and processing of the sections on immunostaining under peroxidase-antiperoxidase techniques have been examined. The tissue fixation in paraformaldehyde solution, removing the resin with sodium ethoxide and enzymatic pronase digestion of the sections resulted in successful specific staining of the antigens. It was found that some cells in fibrous plaques formed a cap of multiple layers of dense connective tissue containing fibronectin and type III, IV and V collagen in the absence of collagen type I.

Adult↗
PubMed1987

An extract of feverfew inhibits interactions of human platelets with collagen substrates.

The interaction of platelets with surfaces coated with collagens of type III (C III) or IV (C IV) has been studied by measuring the deposition of 51-Cr-labeled platelets and by scanning electron microscopy (SEM). Experiments were performed using platelet-rich plasma (PRP) and suspensions of gel-filtered platelets (GFP). Platelets were deposited on C III mainly as surface-bound aggregates. In contrast they were deposited on C IV mainly as spread forms of individual cells. Formation of aggregates on C III was more extensive for PRP than for GFP; in contrast platelet spreading on C IV was more extensive for GFP than for PRP. The effects of an extract of the plant feverfew on platelet-collagen interactions were determined. Feverfew extract inhibited the deposition of 51-Cr-labeled platelets on both C III and C IV in a dose-dependent way. Similar concentrations of extract were needed to inhibit the formation of surface-bound aggregates and to inhibit platelet spreading in both PRP and GFP.

Blood Platelets↗
PubMed1987

Cholesterol regulates high-density lipoprotein interaction with isolated epithelial cells of human small intestine.

The effect of cholesterol on the interaction of high-density lipoprotein (HDL) with isolated human small intestine epithelial cells (enterocytes) was studied. 125I-labeled HDL3 binding by these cells was enhanced in response to cholesterol loading of the cells in a time- and dose- dependent manner. Preincubation of the cells with cholesterol led to the enhancement both of the number of binding sites and the binding affinity. The enhancement of binding correlated with the cellular cholesterol content. Cycloheximide (0.5 mM) inhibited uptake of cholesterol by enterocytes and blocked its effect on 125I-labeled HDL3 binding. The effect of cholesterol on 125I-labeled HDL3 degradation had a double-phase character. At concentrations 10-20 micrograms/ml, the degradation rate was rapidly elevated, but further increase in cholesterol concentration led to a fall in the degradation rate. Incubation of enterocytes with HDL3 resulted in the efflux of cholesterol from cells and its incorporation into HDL3. The results obtained make it possible to assume that binding and degradation of 125I-labeled HDL3 by human enterocytes are independently regulated by the cell total cholesterol content. Binding of HDL by enterocytes may result both in the degradation of HDL and cholesterol efflux from cells.

Cholesterol↗
PubMed1987

Effect of metabolic inhibitors on platelet attachment, spreading and aggregation on collagen-coated surfaces.

The interaction of human gel-filtered platelets (GFP) with surfaces coated with fibrillar calf skin collagen (CSC) or monomeric human type I, III, IV, and V collagen (CI, CIII, CIV, CV) includes both energy dependent and independent stages. Incubation of platelets with a collagen-coated surface at 4 degrees C versus 37 degrees C reduces only shape change and the spreading response of adhering platelets, but does not affect the initial attachment. Additionally, the energy dependence was evident from the reduction of platelet spreading and platelet aggregate formation in the presence of 2-Deoxy-D-glucose (2DG). Antimycin A (AMA), Oligomycin (OM), or 2,4-Dinitrophenol (DNP) did not abolish the adhesion-induced platelet activation, indicating that the energy is supplied by glycolysis rather than by oxydative phosphorylation. In contrast, neither inhibition of glycolysis, nor inhibition of the respiratory chain did affect the initial attachment of nonactivated platelets to the collagen-coated surface. The present data suggest (i) that during the interaction of platelets with collagenous substrates there exists an initial energy independent attachment stage, and (ii) that the following stages of adhesion-induced platelet activation require metabolic energy supported mainly by anaerobic glycolysis.

2,4-Dinitrophenol↗
PubMed1987

Binding of human monomeric type I collagen to platelets.

Interaction of platelets with subendothelial collagen is important in primary hemostasis and thrombosis. Although activation of platelets by collagen polymers has been widely investigated, only insufficient data are available concerning the binding of genetically distinct collagen types in their triple helical (monomeric) form to platelets. We report on the binding of 125I-labeled human type I collagen to platelets. The binding assay was performed at 20 degrees C in the presence of arginine in order to prevent polymerization of the collagen monomers. The binding of monomeric 125I-labeled human type I collagen is dose- and time-dependent, saturable and specific, since it is competitively inhibited by unlabeled type I collagen, but not by unlabeled human type V collagen. Scatchard analysis reveals a class of specific high affinity binding sites with a Kd of 2.5 X 10(-8) M. These results suggest that platelets interact with type I collagen through specific binding sites, and that there are various different binding sites on the platelet membrane for the genetically distinct collagen types.

Binding Sites↗
PubMed1987

Effect of bezafibrate on lipoprotein secretion by cultured human hepatocytes.

The secretion of newly synthesized very low density lipoprotein and low density lipoprotein (VLDL + LDL) and high density lipoprotein (HDL) in cultured human hepatocytes in the presence or absence of bezafibrate added to the culture medium has been evaluated. The content of triacylglycerol, apolipoprotein B, 3H-labeled proteins and 14C-labeled lipids accumulated in a culture medium increased linearly for periods up to 18 h. During incubation, cellular triacylglycerol content was unchanged. This hypolipidemic agent, at a concentration of 10 microM, inhibited secretion of the several VLDL + LDL [3H]apolipoproteins and the VLDL + LDL [14C]lipids, suggesting it can affect the processes of biosynthesis and secretion. The secretion of total [3H]apolipoproteins in the HDL fraction and [3H]protein (d greater than 1.21 g/ml) was unchanged after an exposure to bezafibrate (10 microM). Incubation in the presence of 10 microM bezafibrate resulted also in decreases in both total VLDL neutral lipids and apolipoprotein B secreted into the medium. These results indicate that bezafibrate might exert its plasma lipid-lowering effect by suppressing the VLDL production in liver and reducing the secretion of VLDL into the circulation.

Bezafibrate↗
PubMed1987

[Prevention by alpha and beta adrenoreceptor agonists and lithium hydroxybutyrate of injuries to the endothelium of the rabbit aorta induced by catecholamines].

The damage of endothelial cells and intercellular junctions caused by 10 microM epinephrine (E) and 10 microM norepinephrine (NE) has been observed in perfused rabbit aorta. Simultaneous perfusion of the rabbit aorta with E and NE induced marked endothelial injuries at very low drug doses (0.1 microM). Alpha- and beta-adrenoceptor antagonists prevented the development of catecholamine-induced endothelial alterations. Lithium hydroxybutyrate partially prevented endothelial alterations caused by 10 microM epinephrine, but blocked completely morphological injuries caused by simultaneous perfusion of the rabbit aorta with 0.1 microM E and NE.

Adrenergic alpha-Agonists↗
PubMed1987

Influence of thromboxane receptor-antagonists on the interaction of platelets with solid-phase immobilized human collagen.

The interaction of blood platelets with surfaces coated with human type I, III, IV, and V collagen (CI, CIII, CIV, and CV) has been studied. Using scanning electron microscopy it was demonstrated that the reactivity of the collagen substrates for platelets varies widely. In contrast to CV and CIV, on surfaces coated with CI and CIII, along with spreading, the formation of thrombi-like platelet aggregates occurs. Previously, it was demonstrated that this thrombogenesis in vitro correlates well with the synthesis of platelet prostanoids, and is sensitive to inhibitors of TXA2-synthesis. Therefore, we have investigated the influence of the TXA2/PGH2 receptor-antagonists, 13-azaprostanoic acid (13-APA) and the BM 13.177 compound, on the formation of thrombi-like platelet aggregates on CI and CIII-coated surfaces. It was demonstrated that both 13-APA and BM 13.177 cause a dose-dependent inhibition of the thrombogenesis without any effect on the initiation of the thrombogenesis without any effect on the initial attachment and the spreading of platelets on collagen-coated surfaces. The obtained data suggest that (1) the formation of platelet aggregates on CI and CIII-coated surfaces is triggered by platelet prostanoids; (2) TXA2/PGH2 receptor-antagonists may be useful as antithrombotic drugs.

Blood Platelets↗
PubMed1987

[Effect of rat liver gangliosides on the interaction of liposomes with rat hepatocytes in vitro].

The influence of rat liver GM1, GM2, GD1 and GT1 gangliosides on the interaction of liposomes with rat hepatocytes was investigated. It was shown that liposomes coated with GM1 and GT1 are effectively bound and captured by hepatocytes. Preincubation of hepatocytes with N-acetylglucosamine and D-galactose reduced the binding of GM1- and GT1-liposomes by those cells. The data obtained suggest that there are binding sites for some gangliosides on the surface of rat hepatocytes.

Animals↗
PubMed1986

Enzyme immunoassay of the receptors for modified low density lipoprotein.

Mouse macrophages (line J 774) were incubated with monospecific goat anti-low density lipoprotein antibodies, which were conjugated to horseradish peroxidase (AB-HRP). Addition of low density lipoprotein (LDL) modified by treatment with malondialdehyde to cultures of these cells resulted in a dose-dependent increase in the amount of cell-associated enzyme activity. The concentration curve was hyperbolic with half-saturation of modified LDL at a concentration of about 3 micrograms/ml. This effect was completely blocked by polyinosinic acid and was not observed in experiments with human fibroblasts, which do not exhibit high affinity binding sites that recognize chemically modified LDL. Our data indicate that receptor-mediated endocytosis of AB-HRP in the presence of native or modified LDL may be used as very simple, efficient, and sensitive assay for investigation of the scavenger receptors for modified LDL.

Animals↗