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Biomedical subjects

V S Repin

Publications and source records attributed to V S Repin.

At least 145 records · Page 8Linked to original sources
PubMed1983

Cell proliferation in normal and atherosclerotic human aorta. I. Flow cytofluorometric determination of cellular deoxyribonucleic acid content.

By enzymatic dispersion cells were isolated from intimal and medial layers of healthy and atherosclerotic human aorta. The analysis of cell distribution according to DNA content was made using flow cytofluorometry. It was found that intimal and medial cell populations are heterogeneous with respect to DNA content and include 2 n and 4 n DNA populations. The 4 n cell content may amount to 19% of cell population. As a rule, the percentage of 4 n cells in intima is lower than in media. In atherosclerotic lesions their content is lower than in uninvolved areas. The 4 n-DNA population includes mono- and binuclear cells.

Adult↗
PubMed1983

Cell proliferation in normal and atherosclerotic human aorta. II. Autoradiographic observation on deoxyribonucleic acid synthesis in primary cell culture.

Proliferative potentiality of cells from atherosclerotic and nonatherosclerotic human aorta was evaluated in culture by the incorporation of radioactive thymidine. Thymidine index was determined autoradiographically in primary cultures of intimal and medial cells isolated from zones of fatty infiltration, fatty streaks, atherosclerotic plaques, and uninvolved areas. The thymidine index in medial cultures was higher than in the intimal ones and was unrelated to the type of lesion. In intimal cultures obtained from zones of fatty infiltration and fatty streaks the thymidine index exceeded the normal value by 4.5- and 3-fold, respectively. In cell cultures of the plaque and unaffected intima the thymidine index was the same.

Adult↗
PubMed1982

Flow cytofluorometric study of lipoprotein interactions with cultured endothelial cells.

Accumulation of rhodamine B isothyocyanate-conjugated low density lipoproteins (R-LDL) in cultured endothelial cells from human umbilical cord was studied with a fluorescence activated cell sorter. R-LDL uptake was blocked at 0 degrees C, inhibited by addition of excess of nonlabeled low density lipoprotein, high density lipoprotein-2 or high density lipoprotein-3. High density lipoprotein-2 was about twice as effective in inhibition of R-LDL uptake as high density lipoprotein-3. Endothelial cells that formed a contact-inhibited monolayer lost the ability to incorporate R-LDL via a receptor-mediated pathway. Using R-LDL, it was possible to distinguish cells with different levels of R-LDL incorporation.

Cell Separation↗
PubMed1982

Aortic endothelium of alloxan diabetic rabbits: a quantitative study using scanning electron microscopy.

Scanning electron microscope studies of the aorta and other major arteries have been performed in alloxan-induced diabetic rabbits. After 5 weeks, a variety of structural abnormalities of the endothelial lining were detected including a significant increase in the number of argyrophilic cells and an increased number of craters or openings in the endothelial junctional region. Evidence of more extensive micro-damage was present after 5 months duration of diabetes. These zones with structural changes in the endothelial lining of major vessels seem to be areas of high predilection to atherosclerosis in diabetes.

Animals↗
PubMed1982

Quantitative SEM analysis of injury to the endothelium of rabbit aorta and carotid artery during experimental atherosclerosis.

The luminal surface of the aorta and the carotid artery in normal and cholesterol-fed rabbits (3 weeks, 6 weeks, and 8 months of alimentary hypercholesterolemia) was studied by scanning electron microscopy (SEM). To study endothelial injury the vessels were perfused and stained under physiological pressure. The frequency of large and small endothelial defects was determined per surface unit of endothelium in the normal and experimental groups of rabbits. Loss of endothelial cells was regarded as a large defect, argyrophilic cells, craters, and stomata were regarded as small ones. It was found that the percentage of regions without endothelial cells was similar in both control rabbits and in rabbits with experimental atherosclerosis (0.005--0.04% of the total surface examined). The frequency of small endothelial defects increased in rabbits after 3 weeks of hypercholesterolemia but decreased to the control level after 6 weeks of hypercholesterolemia. In rabbits with 8 months of hypercholesterolemia the frequency and area of defects outside plaques did not differ from the control group. In the group with hypercholesterolemia for 8 months 39.2% of the plaque surface contained endothelial cells in which there were no distinct silver-stained cell borders. Kevex X-ray spectrometric data of silver topography indicated that the plaque surface without distinct cell borders was not an area devoid of cells. The data obtained do not support the assumption that morphological endothelial injury is the structural precursor of plaque formation.

Animals↗
PubMed1982

[RNA content of cells isolated from normal and arteriosclerotic human aorta].

Cells from the intimal and medial layers of the normal and atherosclerotic human aortas were isolated by enzymatic dispersion. The isolated cells were stained in suspension by intravital staining with acridine orange as fluorescent stain for nucleic acids. The intensity of red fluorescence in each cell corresponding to the RNA content was measured and recorded by flow cytofluorometer. Cell distribution as measured by two parameters: red fluorescence (the RNA content) and light scatter (the cell size) revealed two cell subpopulations as regards cell populations from the intima and media, namely A cells with low RNA content and B cells with higher RNA content. The relative cell number in subpopulation A isolated from the intima with atherosclerotic lesions was greater than that isolated from the normal intima.

Adult↗
PubMed1982

[Binding of low density lipoproteins (LDL) to platelets].

Binding of LDL to platelets was studied by two independent methods, radioactive and flow cytofluorimetry, using 125I- and fluorescently labelled RITC-LDL. Saturation of 125I- and RITC-LDL binding to platelets, inhibition of binding by unlabelled LDL and a lower inhibitory effect of unlabelled HDL evidence the existence of a limited number of binding sites specific for LDL in platelets. Unlike nuclear cells platelets do not degrade LDL. The binding of LDL to platelets is reversible and independent of Ca2+. The decrease of total binding level at 4 degrees and the absence of heparin effect on the release of bound LDL suggest LDL incorporation into platelets.

Blood Platelets↗
PubMed1982

[Quantitative analysis of the interaction of low-density lipoproteins with perfused rabbit aorta].

A method for quantitative analysis of interaction between 125I-LDL with perfused rabbit vessels in situ was developed. The method suggested enables the preservation of the integrity of the endothelium in the perfused vascular segment and the study of 125I-LDL incorporation into the affected vessels within the concentration ranges that make possible specific incorporation of LDL into cells. The method can be applied to studying the mechanisms and modulations of LDL uptake by the vascular wall in situ.

Animals↗
PubMed1982

[Detection of 2 cell subpopulations each differing in incorporating low-density lipoproteins in an atherosclerotic plaque from the human aorta].

Cells were isolated by enzyme dispersion of plaques (N-cells) and unaffected areas (A-cells) of human aorta. The capacity of both types of cells to uptake LDL was compared in 7-day primary cultures. Also, these populations were analyzed to discover subpopulations with different types of LDL uptake. RITC-labeled LDL was used for the purpose. A fluorescent-activated cell sorter (FACS-II, Becton and Dickinson, USA) was used to measure the RITC-LDL content and to sort out cell subpopulations. It was shown that the A-cell population consists of two subpopulations with a different type of RITC-LDL uptake. Cells overloaded with lipid inclusions uptake RITC-LDL nonspecifically, while cells without lipid inclusions mostly uptake RITC-LDL through specific receptors.

Adult↗
PubMed1982

[Morphofunctional changes in the endothelial layer of the aorta and carotid artery in rabbits with hypercholesterolemia].

In alimentary hypercholesterolemia in rabbits at the stage preceding the appearance of lipid bands the number of endothelial defects and incorporation of 125I-labeled lipoproteins of low density were significantly increased in the aorta and carotid artery. At the stages of lipid bands and lipid plaques the frequency of endothelial defects and lipoprotein incorporation became normal. The results confirm an important role of the condition of the endothelial tegmentum in the supply of low density lipoproteins into the vessel wall.

Animals↗
PubMed1982

[Lipid metabolism in cells of human atherosclerotic aorta. Study in the primary culture].

Incorporation of 3H-acetate into the main classes of lipids in human aorta cells was studied. It was demonstrated that fractions of intimal and medial cell lipids in primary cultures of unaffected vascular areas were different as to the accumulation of the labeled precursor. Intimal cells isolated from lipid streaks and atherosclerotic plaques accumulated the labeled acetate in lipids 2.5-fold more effectively. The greatest changes in the level of 3H-acetate incorporation were registered in phospholipid fractions and cholesterol esters. Medial cells from the media underlying atherosclerotic lesions were shown to have an enhanced ability to include the label into neutral lipids. It is assumed that the changes in intracellular lipid metabolism may account for the increased lipid content in human atherosclerotic aorta.

Aorta↗
PubMed1981

Human plasma fibronectin promotes the adhesion and spreading of platelets on surfaces coated with fibrillar collagen.

This letter reports that human plasma fibronectin stimulates the interaction of platelets with fibrillar collagen (cell adhesion) and also dramatically changes the shape of adherent platelets, promoting their spreading. The stimulating effect of fibronectin is due to its interaction with collagen fibrils since free fibronectin does not influence the adhesion or spreading of platelets. The results obtained suggest a new physiological function for plasma fibronectin in the control of platelets interaction with damaged vessel walls.

Blood Platelets↗
PubMed1981

Endothelial cell culture on fibrillar collagen: model to study platelet adhesion and liposome targeting to intercellular collagen matrix.

Human umbilical endothelial cells (ECs) were grown on fibrillar type I collagen in 16.4-mm multiwell tissue culture plates. Human platelets were added to the wells, and platelet adhesion to collagen was examined by scanning electron microscopy and radioisotopic technique in the absence of ECs and in preconfluent and confluent EC cultures. Single adherent platelets of different shapes as well as small aggregates were seen on collagen surface. Human plasma fibronectin added to the system stimulated platelet adhesion and their spreading on collagen. ECs had no effect on the percentage of platelets adherent to collagen-coated gaps in preconfluent culture but decreased the number of spread platelets. It is demonstrated that collagen-coated gaps can bind 14C-labeled liposome--antibody and 14-C-labeled liposome--fibronectin conjugates. ECs grown on fibrillar collagen are suggested as useful models for screening of antiplatelet drugs and for the study of drug targeting to the areas of vascular injury for prevention of thrombosis.

Blood Platelets↗
PubMed1981

[Primary culture of endothelial cells from the human umbilical vein: identification and characteristics of a growing and confluent culture].

Endothelial cells (EC) were derived selectively from the intimal surface of human umbilical veins with a 0.1% collagenase solution, after Gimbrone et al. (1974) with some modifications. The plating efficiency to plastic was 70-75% for 24 hours in collagenase dispersed cells. A confluent monolayer with cell density 10(5) cells/cm2 as formed by 5-8 days. The optimal cell growth was obtained with seed density 5-8 X 10(4) cells/cm2. The EC were identified in culture using the following hallmarks: a) the presence of the Weibel-Palade bodies in the cytoplasm, b) VIII coagulation factor, c) silver staining of EC borders in monolayer. The EC doubling time in the log phase of growth was shown to be 48-56 hours. The contact DNA inhibition was demonstrated in confluent culture with 3H-thymidine incorporation and by means of a cell flow-cytofluorometry method. The same methods were used for evaluating the homogeneity of EC in culture.

Cells, Cultured↗
PubMed1981

[Quantitative study of endothelial defects in the aorta and carotid artery in experimental atherosclerosis].

The inner surface of the aorta and carotid artery in normal rabbits (group 1) and after 3 weeks (group 2), 6 weeks (group 3) and 8 months (group 4) of hypercholesterolemia was studied by scanning electron microscopy. In all the cases the area of de-endothelialized zones was equally small. Incidence of microdefects in the endothelium (argyrophilic cells, craters and stomata) increased in group 2, but decreased in group 3 and group 4 (outside the plaques). No typical endothelium with argyrophilic borders was observed on 39.2% of the plaque surface in group 4, though the cells were present. The data obtained show that vast zones of de-endothelialization do not precede the development of atherosclerotic plaques.

Animals↗