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Biomedical subjects

E M Tararak

Publications and source records attributed to E M Tararak.

At least 19 recordsLinked to original sources
PubMed2004

[Expression of urokinase plasminogen activator, its receptor and plasminogen activator inhibitor type 1 in different types of atherosclerotic lesion in human aorta].

The role of plasminogen activators in the regulation of key processes of atherosclerosis progression stays unclear. The aim of this study was to evaluate the expression of urokinase plasminogen activator (uPA), its receptor (uPAR) and the plasminogen activator inhibitor type 1 (PAI-1) in human aorta, and to balance them with the stage of atherosclerotic lesion. We have shown that uPA and uPAR in normal aorta are mostly expressed by intimal smooth muscle cells. The expression of these proteins was up-regulated in diseased aorta compared to normal artery. The most part of cells in both fatty streak and fibro-fatty lesion were monocytes/macrophages, and about 60% of these cells expressed uPA and its receptor. PAI-1 was mostly localized on the lumonal part of the aorta and in the extracellular matrix of the intima. We observed a moderate increase of PAI-1 expression in atherosclerotic lesion. Thus, our data indicate participation of plasminogen system in atherogenesis.

Adult↗
PubMed2003

[The origin of neointimal cells in the rat carotid artery after balloon angioplasty].

At present the issue of a possible role of circulating stem cells and precursors in pathological vascular wall remodeling after angioplasty remains unsolved. Therefore the origin of neointimal cells was examined in the rat carotid artery after balloon angioplasty using morphological and immunocytochemical approaches. It is shown that at the early stages (1-7 days) after vessel injury acute inflammatory response arises in the arterial wall recruiting neutrophils, monocytes, macrophages as well as large amounts of low-differentiated blood-derived cells. At the late stages (10-28 days), at the area of injured intima, a new hyperplastic intima (neointima) is formed, which consists of cells carrying specific smooth muscle markers--alpha-actin and smoothelin. The study on cell proliferative behaviour in the injured vessel wall by bromodeoxyuridine showed that in the process of neointima formation blood-born rather than resident cells are involved. Probably, early smooth muscle and endothelial precursor cells penetrate into injured area with blood stream, where they proliferative and differentiate into mature cells.

Angioplasty, Balloon↗
PubMed2002

Proliferative activity and expression of cyclin-dependent kinase inhibitor p21WAF1 and p53 protein in endothelial cells of human aorta during replicative aging in vitro.

Experiments with bromodeoxyuridine showed that the count of nonproliferating cells in a monolayer culture of aortic endothelial cells from adult humans rapidly increased during long-term subculturing. Cytochemical assay showed that these cells contain neutral b-galactosidase, the marker of aging cells. Immunocytochemical assay demonstrated that most cells express p53 protein and inhibitor of the cell cycle p21WAF1.

Adult↗
PubMed2002

Sialidase activity in normal and atherosclerotic human aortic intima.

Sialidase activity has been determined in homogenates of human aortic intima by measuring the amount of GM1 formed during the incubation of ganglioside GD1a with the tissue homogenates. Areas with atherosclerotic lesions as well as adjacent areas without histological evidence of atherosclerosis were taken for comparison. The rate of GM1 formation from GD1a in the presence of homogenates of the atherosclerotic intima was 20 pmol/h per mg protein. Homogenates of the unaffected intima did not desialylate GD1a. Sialidase activity of the atherosclerotic intima was linear for 1.5 h at GD1a content up to 1.5 nmol and at homogenate protein up to 1 micro g. NH4Cl and NeuAc2en, inhibitors of lysosomal function and plasma membrane-bound sialidase, respectively, reduced sialidase activity of homogenates of the atherosclerotic intima by 94%. The results indicate that atherosclerotic lesions and unaffected intima differ in their activity and specificity of sialidases that cleave gangliosides.

Adult↗
PubMed2002

[Expression of T-cadherin in the rat carotid artery wall after balloon injury and in different rat organs].

T-cadherin is an unusual glycosilphosphatidylinositol (GPI)-anchored member of the cadherin family of cell adhesion proteins. In contrast to classical cadherins, tissue distribution of T-cadherin so far remained unknown. We examined tissue distribution of T-cadherin in rats using Western blotting and immunohistochemical method. Our results show that T-cadherin is expressed in all types of muscles (cardiac, striated, and smooth muscles), in brain neurons, and spinal cord, in the vessel endothelium, at the apical pole of intestinal villar epithelium, in the basal layer of skin, and eosophagal epithelium. Blood-derived and lymphoid cells as well as connective tissue were T-cadherin-negative. The highest level of T-cadherin expression was revealed in the cardiovascular system. Although T-cadherin was detected in smooth muscle cells, its role in the intimal thickening and restenosis is not known. We examined T-cadherin expression within 1-28 days after balloon injury of rat left carotid arteries. T-cadherin expression was valued immunohistochemically with semiquantitative method. In uninjured arteries, T-cadherin was expressed in endothelial (vWF-positive) cells, and smooth muscle (alpha-actin-positive) cells (SMCs). After denudation of arterial wall, T-cadherin was present both in the media and neointima. We revealed dynamics of T-cadherin expression in the media of injured artery: an essential increase being registered at the stage of cell migration and proliferation in the media and neointima (1-7 days), followed by its decrease to the baseline level (10-28 days). The high upregulation of T-cadherin expression in the media and neointima during migration and proliferation of vascular cells after vessel injury enables us to suggest the involvement of T-cadherin in vessel remodeling after balloon catheter injury.

Angioplasty, Balloon, Coronary↗
PubMed2001

Sialyltransferase activity in normal and atherosclerotic human aorta intima.

Sialyltransferase activity has been determined in Golgi membrane fractions isolated from atherosclerotic and normal intima of human aorta by measuring the transfer of N-acetylneuraminic acid (NeuAc) from CMP-NeuAc to asialofetuin. The asialofetuin-sialyltransferase activity was found to be twofold higher in the atherosclerotic intima than in the normal intima. The mean value of the apparent Michaelis constant (Km) for the sialylating enzyme in both tissues did not differ and was 57 microM. In contrast, the maximal velocity (Vmax) was 2-fold higher for the atherosclerotic intima than for the normal intima. These results suggest that expression of asialofetuin-sialyltransferases of the aortal intima may be increased in atherosclerosis.

Adult↗
PubMed2001

Effects of transforming growth factor-beta(1)on proliferation of smooth muscle cells in human aortic intima and human promonocytic leukemia THP-1 cells.

We studied the effects of transforming growth factor on proliferation of cultured smooth muscle cells from human aortic intima and proliferation and differentiation of human leukemia THP-1 promonocytes. Transforming growth factor inhibited proliferation of these cells, but stimulated differentiation of THP-1 cells. Therefore, transforming growth factor probably modulates proliferation and differentiation of smooth muscle cells and monocytes/macrophages involved in the pathogenesis of atherosclerotic damages.

Aorta↗
PubMed1993

[Population kinetics of circulating monocytes in health and in patients with ischemic heart disease].

Population kinetics of monocytes (MC) was studied to prove their participation in atherogenesis. Increased number of cells containing lipids (CCL) in patients with severe stable angina pectoris is demonstrated (42.5 versus 7.4% in healthy persons). This is followed by MC esterase activity enhancement. In patients with angina of effort new types of MC appear (with high peroxidase and low esterase activity) and there is a drastic increase of CCL (more than 56%). The correlation between the number of CCL and indices of blood lipid metabolism in anginal patients is lacking. The results obtained may serve as a criterion for evaluating the degree and exacerbation of coronary atherosclerosis in humans.

Adult↗
PubMed1991

The expression of skin-specific gene K51 in the epidermal layer of human skin and in basal cell carcinoma cells.

Gene K51 probe isolated previously from the rat genomic library has been used to study the expression of its human counterpart by in situ hybridization and Northern blot analysis. A polyA-containing transcript of human gene K51 of 3 kb size has been detected in embryonic skin. The gene is also expressed in the epidermis of newborn humans and adults, but not in the adjacent mesenchymal tissues. Immunostaining with keratin antisera revealed predominantly earlier stage expression of K51 than cytokeratin markers. Sebaceous and sweat glands also contain cells expressing K51 gene. K51 expression was found in the cells of eight individual basal cell carcinomas tested, with the level of expression lower than in keratinocytes from normal human epidermis. We propose that K51 gene expression could serve as a convenient marker for the study of the process of skin keratinocyte development and the changes in this process associated with skin cancers and dysplasia.

Blotting, Northern↗
PubMed1991

[Monocyte-macrophage infiltration in portions of atherosclerotic lesions of the human aorta].

Human thoracic aorta was taken from trauma victims aged from 6 to 40 years. Cell composition of the intimal layer was investigated in the lesion predisposed (LP) areas of the aorta and in the lesion resistant (LR) areas. By double immunofluorescent staining with mono and polyclonal antibodies to monocytes/macrophages (Mn/Mph) and smooth muscle cells (SMC) the presence of Mn/Mph was revealed in all aortas studied. The number of these cells was 2-6 fold higher in LP areas, compared to LR areas in all persons over 21 years of age. Scanning electron microscopy revealed Mn on the luminal surface of the vessel the number of which was frequently higher in LP areas. Mn/Mph in LP areas were heterogeneous in their structure depending on the depth of their localization in the intima. The revealed Mn/Mph infiltration in aortas of young subjects may be the earliest manifestation of the atherosclerotic lesion.

Adolescent↗
PubMed1991

[Structure of the neointima after balloon catheter injury of the rabbit aorta in the context of hypercholesterolemia: analysis of endothelial influence on lipid accumulation].

Balloon catheter de-endothelialization of abdominal aorta of cholesterol-fed rabbits was performed. As a result, partly endothelialized neointima was formed, consisting of smooth muscle cells and macrophages. Neutral lipids stored more intensely in non-endothelialized part of neointima. Preferential intracellular lipid accumulation in this area was observed while predominantly extracellular lipid accumulation was found in endothelium-covered part of neointima. It is supposed that endothelium inhibits intracellular lipid accumulation and at the same time stimulates an extracellular one, but as a whole it reduces the density of lipid inclusions in neointima.

Animals↗
PubMed1990

Visualization of apo B, fibrinogen/fibrin, and fibronectin in the intima of normal human aorta and large arteries and during atherosclerosis.

Apolipoprotein B (apo B), fibrinogen/fibrin, blood platelets, factor VIII-related antigen of the blood coagulation system, and smooth muscle cells (SMC) were identified in the intima of normal and atherosclerotic human aorta and large arteries by the indirect immunofluorescence technique. Fibrinogen/fibrin was revealed by a monoclonal antibody (monAb) against the C-terminal region of human fibrinogen A alpha-chain. Fibronectin was visualized by monAb to the cellular form and against an epitope shared by different fibronectin subunit variants. In normal intima, fatty streaks, small amounts of fibrinogen/fibrin together with large amounts of apo B were observed. Fibronectin detected by two types of monAb was not found in extracellular matrix (ECM), whereas cellular fibronectin encircled SMC. According to the data obtained, fibrinogen/fibrin accumulates in plaques as a result of intramural thrombus incorporation, blood insudation, intramural haemorrhage, and in or around cells, apparently macrophages.

Aged↗
PubMed1990

Localization of apolipoprotein E in normal and atherosclerotic human aorta.

To elucidate the role of apolipoprotein E (apo E) in atherogenesis, we have investigated the localization of apo E in normal and atherosclerotic aortas as well as in other tissues of 32 post-mortem individuals. Using double immunofluorescence it has been found that normal intima of individuals older than 20 years and some adolescents contained immunoreactive material that reacted with poly- and monoclonal antibodies to apo E. A staining pattern of apo E differed from that of apolipoprotein B, the latter being seen in normal intima of each child older than 7 years. Apo E was present extracellularly in lipid streaks and atheromatous plaques, where its staining was particularly intensive around the necrotic zone of plaques. Some macrophages in the plaques of 4 aortas exhibited apo E-positive staining, while aortic endothelial and smooth muscle cells never contained apo E. Apo E-positive staining was not found in the majority of vessel cells, it was always, however, observed in other types of cells including hepatocytes. Kupffer cells, spleen macrophages and cerebral astrocytes. Our findings indicate that only some macrophages in human aorta may be responsible for the production of apo E that can participate in reverse cholesterol transport. At the same time, apo E accumulation in the aortic wall may promote the development of atherosclerosis.

Adolescent↗