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Biomedical subjects

E M Tararak

Publications and source records attributed to E M Tararak.

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

Heterogeneity of smooth muscle cells in atheromatous plaque of human aorta.

This study was undertaken to investigate the expression of cytoskeletal proteins and the ultrastructure of cells in normal intima and atheromatous plaque of human aorta. It has been established, using double-labeling immunofluorescence, that smooth muscle cells (SMC) in normal aortic intima contain myosin, vimentin, and alpha-actin but do not react with antibodies against desmin. In contrast, 7 of 28 atherosclerotic plaques contained many cells expressing desmin in addition to the other cytoskeletal proteins characteristic of normal intima SMC. These cells were localized predominantly in the plaque cap and had the ultrastructural features of modulated SMC, ie, well-developed endoplasmic reticulum and Golgi apparatus. Besides, some cells in the 13 atherosclerotic plaques proved to be myosin, alpha actin, and desmin negative but contained vimentin and actin as revealed by fluorescent phalloidin. These cells were found in the immediate proximity of atheromatous material and reacted with a monoclonal antibody specific to SMC surface protein (11G10) but not with monoclonal anti-muscle actin (HHF35) and anti-macrophage (HAM56) antibodies. Electron microscopy of this plaque zone revealed that the cytoplasm of these cells was filled with rough endoplasmic reticulum and a developed Golgi complex. At the same time, a certain proportion of cells in this region retained morphologic features of differentiated SMC such as the presence of a basal lamina and myofilament bundles. The revealed peculiarities of cytoskeletal protein expression and the ultrastructure of cells in human aortic atherosclerotic plaques may be explained by a phenotypic modulation of vascular SMC.

Adolescent↗
PubMed1990

[Apo B, fibrinogen-fibrin and fibronectin in the intima of the normal human aorta and large arteries and in atherosclerosis].

Apo B, fibrinogen/fibrin, fibronectin, thrombocytes, factor VIII of the blood coagulation and smooth muscle cells (SMC) were identified by the immunofluorescence method in the intima of aorta and big arteries under normal conditions and in atherosclerosis. Monoclonal antibodies (MCA) against C-end fragments of A alpha-fibrinogen chain were used in the study of fibrinogen/fibrin. MCA reacting with plasma fibronectin and those reacting with A-area of the polypeptide chain specific for the cell fibronectin were used for the identification of fibronectin. Small amount of fibrinogen/fibrin, no fibronectin in the extracellular matrix and the cell fibronectin around SMC were observed on the normal intima and lipid strip in spite of the presence of Apo B. The results indicate that fibrinogen/fibrin is accumulated in the plaques due to the incorporation of the wall thrombi, insudation from the blood plasma, intramural haemorrhages as well as around cells, presumably macrophages.

Adult↗
PubMed1990

[Phenotypic variants of the smooth-muscle cells in an atheromatous plaque of the human aorta].

The authors investigated the expression of cytoskeletal proteins and the ultrastructure of cells in normal intima and atheromatous plaque of human aorta. It has been established, using double immunofluorescent method and a set of antibodies that intimal smooth muscle cells /SMC/ of normal aorta express myosin, vimentin, alpha-actin and actin but not desmin. In seven out of 28 atherosclerotic plaques the cells contained desmin and all other SMC cytoskeletal proteins were found. These cells had the ultrastructural features of SMC, i.e. well-developed endoplasmic reticulum and Golgi apparatus. Besides, some cells in 13 atherosclerotic plaques proved to be myosin-, alpha-actin- and desmin-negative. The cells were stained with monoclonal antibodies specific to SMC but not with macrophage-specific antibody. Ultrastructurally, the cytoplasm of the cells was filled with rough endoplasmic reticulum and a developed Golgi complex, but a certain portion of the cells retained basal lamina and myofilament bundles. The peculiarities of cytoskeletal protein in expression and ultrastructure of cells in human aortic atherosclerotic plaques may be explained by a phenotypic modulation of vascular SMC.

Adolescent↗
PubMed1990

[The localization of apoprotein E in the normal human aortic wall and in atherosclerosis].

The authors studied the distribution of apoprotein E (apoE) in normal and atherosclerotic human aortic wall. Double immunofluorescent technique and a set of mono- and polyclonal antibodies were used in the study. Apo E was found in normal intima of every aorta taken from people over 20 years of age and in vessels of some adolescents. The protein was localized extracellularly and was noted in some portion of macrophages but not in the endothelial and smooth muscle cells of human aorta. The accumulation of apo E increased in lipid strips and was particularly high in acellular zone of the atherosclerotic plaque. This effect may be due to the retention of apo E by changed sulfated glycosaminoglycans of aortic connective tissue. The accumulation of apo E in the vessel wall may have an important role in the pathogenesis of atherosclerosis.

Adolescent↗
PubMed1990

[Immunocytochemical analysis of apoprotein E distribution in human tissues].

Localization of apoprotein E (apo E) has been studied in different human tissues. For this aim the immunoperoxidase method and peroxidase-antiperoxidase complex, polyclonal and monoclonal antibodies, to apo E have been used. In every human tissue analysed apo E-containing cells have been revealed. To the latter the following cell types belong: hepatocytes and hepatic sinusoidal cells, macrophages of the spleen, lymph nodes and pulmonary tissues, glial cells and cells in all layers of the adrenals, skin keratinocytes, cells of the glomerular capsule and convoluted tubules of the kidney, spermatocytes and smooth muscle cells of the testis. Besides, apo E is revealed in endothelium of some vessels. As demonstrate the results obtained, apo E is found practically in all human tissues. A suggestion is made that besides its participation in reverse cholesterol transport, this protein performs a number of additional functions, such as regulation of local hormonal homeostasis of an organ.

Adult↗
PubMed1989

[Immuno-morphologic detection of specific APO-B antigenic determinants in normal intima and atherosclerotic plaques in the human aorta].

Various apo-B antigenic determinants exposures in the normal aortic intima and atherosclerotic plaques were examined by immunofluorescence using 5 clones from monoclonal antibodies (BAb) to apo-B. As a rule, 4 clones were found to react with apo-B in the normal aortic intima, whereas the clone 12G10 failed to respond to it. All the 5 determinants of apo-B were exposed in the fibrous tissue of most atherosclerotic plaques. However, there were atherosclerotic plaques, in whose fibrous tissue only did 1 to 3 clones positively react with apo-B. The similar expression of apo-B antigenic determinants was observed in the atheronecrotic zone of fibrous plaques. Apo-B did not respond to apo-B MAb at all in some atherosclerotic plaques present in the zone of atheronecrosis. Whether it is possible to modify low-density lipoproteins just in the arterial wall, especially in atherosclerotic plaques and whether this process is significant in the pathogenesis of atherosclerosis are discussed in the paper.

Adult↗
PubMed1989

[The age-related dynamics of the distribution of prelipid changes and lipoidosis in the human aortic intima].

The aortas of 22 practically healthy persons who died accidentally at the age of 20 to 60 years and 112 patients with atherosclerosis dying from the complications of the ischaemic heart disease (IHD) at the age of 30 to 80 years were studied by macroluminescent analysis. The incidence and distribution of prelipid changes (PC) in the intima were compared to those of lipidosis. PC of the type of a simple oedema, gelatinous plaque or muscular-elastic hyperplasia extinguish the primary fluorescence and macroscopically look as areas having the shades of a blue colour. The spread of PC in the aorta depends on the age and the degree of atherosclerosis. A significant increase of the PC surface in the aorta of persons dying from IHD as compared to the healthy persons indicate the exacerbation of the atherosclerotic process. The type and the gravity of the atherosclerosis in the human aorta are determined by the qualitative and quantitative correlations of PC and lipidosis.

Adult↗
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

[Receptor-mediated mechanism of catecholamine damage of the endothelium of major arteries].

In 20 rabbits, the mechanism responsible for receptor-mediated lesion and desquamation in the endothelium was studied during isolated aortic perfusion. The screening of catecholamines, artificial adrenoceptor agonists and agents simulating the action of secondary messengers indicated that simultaneous activation of alpha- and beta-adrenoceptors resulted in endotheliocyte death and increased aortic wall permeability. Subsequently, the vasoactive agents entering as a component of transudate the medial aortic tunic caused persistent smooth muscle cell spasm. The resultant compressing tensions of the collagenoelastic carcass of the aorta led to the removal of the transudate from the medial tunic into the subendothelial space through the fenestras of the internal elastic membrane. The removable liquid detached impaired endothelial layers from the membrane surface and lifted it off, forming local distended areas. These areas were torn off by blood flow, uncovering the surface of the internal elastic membrane.

Animals↗
PubMed1988

Agonist-induced polyphosphoinositide breakdown in cultured human endothelial and vascular smooth muscle cells.

Human aortic endothelial cells and smooth cells (SMC) from human aorta and coronary arteries were grown in culture. Subcultured vascular SMC retained several important features of human vascular SMC in situ, for example, vimentin-type intermediate filaments, smooth muscle myosin, a well-developed microfilament system, and expression of caldesmon protein involved in the regulation of contraction in smooth muscle. Aortic endothelial cells were shown to possess functional receptors to histamine, thrombin, serotonin, acetylcholine, bradykinin, platelet activating factor (PAF), angiotensin II, vasopressin, prostaglandin E2 (PGE2), and U46619, a stable analog of thromboxane A2. All these substances stimulated polyphosphoinositide (PPI) breakdown in endothelium. Thrombin, histamine, and PAF were the most potent activators. The response of aortic SMC to the same panel of agonists were different. Serotonin, histamine, and angiotensin II produced higher levels of inositol phosphates (IP, IP2, IP3) in SMC than in endothelium. Responses to acetylcholine, bradykinin, and PGE2 were weak and inferior to those of endothelial cells. Other agents evoked approximately equivalent responses in both cell types. Coronary artery SMC resembled aortic SMC in the high extent of PPI hydrolysis after stimulation with serotonin and histamine. The complete inability of angiotensin II and vasopressin to cause accumulation of inositol phosphates in coronary SMC contrasted with the presence of functional receptors to these hormones on aortic SMC. We conclude that the effect of vasoactive agents on human vascular cells may be realized via activation of PPI hydrolysis. Agonists with reported strong vasoconstrictor action seem to stimulate preferential PPI hydrolysis in SMC, whereas endothelium-dependent relaxers cause more pronounced PPI breakdown in endothelial cells. Peculiarities of angiotensin II and vasopressin receptor expression and/or coupling in human aorta and coronary artery SMC may be relevant for understanding the selective action of agonists on human vessels.

Aorta↗
PubMed1988

[Dynamics of lipid accumulation on human aortic walls in atherosclerosis].

The authors studied distribution of apoprotein B (apo B) and lipids containing esterified and nonesterified cholesterol (EC and NEC) in human aortic wall, using methods of indirect immunofluorescence with antibodies of apo B, and filipin and oil red 0 staining. All the examinees over 14 exhibited visually intact and atherosclerosis-affected vascular sites of accumulated apo-B-containing lipoproteins. EC, staining oil red 0, occurred only in the lipid strip and atherosclerotic plaque. Filipin-positive NEC was found in atherosclerotic plaque only. NEC disseminated extracellularly in the form of separate spherical corpuscles and homogenously. Saline pretreatment of nonfixed cryostat sections reduced the intensity of filipin homogenous staining. Mechanisms of lipids formation in vascular tissue of humans are under discussion.

Adolescent↗
PubMed1988

[Polymorphism of smooth muscle cells in atheromatous plaques of the human aorta].

The expression of cell cytoskeleton proteins in atheromatous plaques of human aorta was investigated using double immunofluorescence technique and a set of antibodies. It was found that in 4 out of 12 plaques some smooth muscle cells (SMC) were stained by monoclonal antibodies to desmin. No such cells were detected in apparently unaffected aortic intima. In addition to typical SMC and these cells, the cells unstained by antisera to smooth muscle myosin but reacting with monoclonal antibodies to vimentin and SMC surface were revealed in all plaques adjacent to the central fatty mass.

Adult↗
PubMed1987

[Immunohistochemical and histoenzymological characteristics of the arterial intimal cells in nonspecific aorto-arteritis].

Enzymatic activity of cells, antigenic cellular markers and extracellular matrix of the hyperplastic intima of the aorta and carotid arteries was investigated in non-specific aorto-arteritis by immunomorphological and histochemical techniques. The cells of subendothelial layer of thickened arterial intima contained smooth muscle cell myosin, gave positive reactions to myosin ATP-ase and revealed high activity of thiamine pyrophosphatase. Fibronectin and type IV and V collagen were located in close proximity to these cells. The data obtained make it possible to consider these cells as modified smooth muscle cells. Type III collagen was the prevalent type of extracellular matrix of the thickened intima. A great number of blood vessels of the capillary and precapillary types have been found to penetrate into the intima from the adventitia. A possible role of pericytes surrounding newly formed capillaries as the precursors of subendothelial cell population in the hyperplastic intima is discussed.

Adenosine Triphosphatases↗
PubMed1986

[Effect of chalone-containing aorta extracts on regression in experimental atherosclerosis].

The effect of chalone-containing aortic extracts on proliferative activity of smooth muscle cells was examined in conditions of experimental hypercholesterolemia. The tissue-specific cell proliferation inhibitor present in the extract is shown to depress mitotic activity of smooth muscle cells in postnatal rats. The area under aortic atherosclerotic lesion diminished twofold as compared to that of the controls. Morphologically, atherosclerotic changes are seen as lipid plaques.

Animals↗
PubMed1984

[Dynamics of the activity of lysosomal and membrane-transport enzymes of human coronary arteries in atherosclerosis (based on specimens of early autopsy].

The time course of the activity of lysosome (LE) and membrane-transport (MTE) enzymes in the cells of human coronary arteries was studied histochemically and lipid metabolism in the plasma was studied biochemically. it is shown that the formation of atherosclerotic lesions and exacerbation of the disease in the endothelium and macrophages is followed by the enhancement of positive correlation between the atherogenic ration and the activity of LE and MTE and the alteration of this correlation between these enzymes. In the sedentary mesenchymal cells the progress of atherosclerosis results in the alteration of positive correlation between both LE and MTE and between these enzymes and atherogenic ration. Atherosclerosis remission is followed by partial restoration of the above correlations between the activity of LE and MTE in the cells of atherosclerotic lesions of the coronary arteries intima.

Acetylesterase↗
PubMed1983

[Quantitative histoenzymological and biochemical studies of the stages of atherogenesis in human coronary arteries (based on the data of early autopsies].

Histochemical methods were used to study the dynamics of activity of energetic metabolism enzymes (EME) in cell elements of the human coronary artery (CA) wall in comparison with biochemical values of lipid metabolism in the plasma. The development of CA atherosclerosis was shown to be determined to a large extent by reciprocal relations of antiatherogenic alpha-lipoproteins and atherogenic beta-lipoproteins in their influence on EME activity. An increased EME activity at early stages of atherogenesis (lipid plaque) is an adaptation to changed homeostasis. The lipid plaque is a turning point in the process of metabolic adaptation. Evolution of atherosclerotic changes is accompanied by disjunction and transformation of correlative connections between EME activity in CA wall cells.

Adenosine Triphosphatases↗