Immunohistochemical Detection of Apolipoprotein A-I and B-100 in Canine Atherosclerotic Lesions

2003 ◽  
Vol 40 (3) ◽  
pp. 328-331 ◽  
Author(s):  
T. Sako ◽  
E. Uchida ◽  
Y. Kagawa ◽  
K. Hirayama ◽  
T. Nakade ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Coronary Arteries ◽  
Peripheral Arteries ◽  
Immunohistochemical Detection ◽  
Atherosclerotic Lesions ◽  
Apolipoprotein A ◽  
Subendothelial Space ◽  
Immunohistochemical Techniques ◽  
Tunica Intima

We attempt to determine and compare the localization of apolipoproteins (apo) apoA-I and B-100 in atherosclerotic lesions of canine aortas, coronary arteries, and the peripheral arteries, using immunohistochemical techniques. Histopathologically, atherosclerotic lesions were characterized by deposition of lipids and infiltration of lipid-laden foamy cells in the tunica intima and tunica media, sometimes forming fibrofatty plaques containing abundant sudanophilic and mineralized material. Canine apoA (CapoA)-I and canine apoB (CapoB)-100 immunopositive signals were simultaneously observed in mild and severe atherosclerotic lesions of the aorta, coronary arteries, splenic arteries, and renal arteries in the double-immunolabeled sections. Both CapoAI and CapoB-100 positive signals were seen in the cytoplasm of endothelial cells, smooth muscle cells, and macrophages. The subendothelial space and extracellular matrix in the tunica intima and media were also positive. Neither CapoA-I nor CapoB-100 positive signals were seen in normal arteries. These findings closely resemble those of the localization of apoA-I and apoB-100 in human atherosclerotic lesions.

scholarly journals Hybrid technologies in surgical treatment of patients with concomitant atherosclerotic lesions of carotid and coronary arteries

2015 ◽  
Vol 17 (1) ◽  
pp. 45 ◽  
Author(s):  
A. M. Chernyavskiy ◽  
M. A. Chernyavskiy ◽  
T. Ye. Vinogradova ◽  
A. G. Yedemskiy
Keyword(s):  
Surgical Treatment ◽  
Coronary Arteries ◽  
Carotid Arteries ◽  
Rapid Development ◽  
Peripheral Arteries ◽  
Endovascular Techniques ◽  
Hybrid Procedures ◽  
Atherosclerotic Lesions ◽  
Hybrid Technologies ◽  
Revascularization Surgery

Cardiovascular diseases, which have their origins in atherosclerosis, are the "leaders" in morbidity and mortality among the population in many countries. Given the increase of elderly people in the population, it is important to choose the best strategy for surgical treatment of patients with combined atherosclerotic lesions of several arteries (coronary arteries, carotid arteries, peripheral arteries of the lower extremities, atherosclerosis visceral branches of the abdominal aorta). Currently, there is yet no common approach to the timing and sequence of revascularization surgery in this group of patients. The rapid development of endovascular techniques enables us to carry out the so-called hybrid procedures in patients with atherosclerotic lesions of several arteries. In this article we analyze different strategies that are used to manage patients with both coronary and carotid arteries atherosclerotic lesions.

scholarly journals Bridging Coronary Physiology into Clinical Application of Acute Coronary Syndrome

Arkus ◽  
2021 ◽  
Vol 5 (1) ◽  
pp. 195-197
Author(s):  
Hardi Darmawan
Keyword(s):  
Acute Coronary Syndrome ◽  
Coronary Arteries ◽  
Stress Factors ◽  
Coronary Physiology ◽  
Tunica Media ◽  
Coronary Syndrome ◽  
Atherosclerotic Lesions ◽  
Heparin Sulfate ◽  
Coronary Syndromes ◽  
Tunica Intima

Normal arteries have three layers of structure, tunica intima, tunica media, and tunica adventitia. Intima tunica is the deepest layer of coronary arteries in which there are antithrombotic molecules such as heparin sulfate, thrombomodulin, and plasminogen activator. In addition, tunica intima also contains substances that regulate the contraction of tunica smooth muscle cell media, called nitric oxide (vasodilators) and prostacyclin (vasoconstrictors). Tunica intima and tunica media seem to be directly related to the atherosclerosis process. Meanwhile, the role of tunika adventisia is unknown. The accumulation of atherosclerotic lesions and hemodynamic stress factors and the degradation of extracellular matrix will cause susceptibility of atherosclerotic plaque fibrous capsules to rupture and form thrombus. Thrombus that occurs in the coronary condition causes acute coronary syndrome, characterized by typical symptoms such as chest pain depending on the thrombus formed. In studying acute coronary syndromes, of course it cannot be separated from understanding the physiology of coronary arteries and the process of atherosclerosis. Therefore, this article aims to briefly explain coronary physiology.

scholarly journals Pathogenesis of atherosclerosis in the tunica intima, media, and adventitia of coronary arteries: An updated review

2019 ◽  
Author(s):  
Aleksandra Milutinović ◽  
Dušan Šuput ◽  
Ruda Zorc-Pleskovič
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
Muscle Cells ◽  
Chronic Inflammatory Disease ◽  
Elastic Membrane ◽  
Atherosclerotic Plaques ◽  
Perivascular Adipose Tissue ◽  
Tunica Intima

Atherosclerosis is a chronic inflammatory disease of arteries and it affects the structure and function of all three layers of the coronary artery wall. Current theories suggest that the dysfunction of endothelial cells is one of the initial steps in the development of atherosclerosis. The view that the tunica intima normally consists of a single layer of endothelial cells attached to the subendothelial layer and internal elastic membrane has been questioned in recent years. The structure of intima changes with age and it becomes multilayered due to migration of smooth muscle cells from the media to intima. At this stage, the migration and proliferation of smooth muscle cells do not cause pathological changes in the intima. The multilayering of intima is classically considered to be an important stage in the development of atherosclerosis, but in fact atherosclerotic plaques develop only focally due to the interplay of various processes that involve the resident and invading inflammatory cells. The tunica media consists of multiple layers of smooth muscle cells that produce the extracellular matrix, and this layer normally does not contain microvessels. During the development of atherosclerosis, the microvessels from the tunica adventitia or from the lumen may penetrate thickened media to provide nutrition and oxygenation. According to some theories, the endothelial dysfunction of these nutritive vessels may significantly contribute to the atherosclerosis of coronary arteries. The adventitia contains fibroblasts, progenitor cells, immune cells, microvessels, and adrenergic nerves. The degree of inflammatory cell infiltration into the adventitia, which can lead to the formation of tertiary lymphoid organs, correlates with the severity of atherosclerotic plaques. Coronary arteries are surrounded by perivascular adipose tissue that also participates in the atherosclerotic process.

scholarly journals Features of atherosclerotic lesions of the coronary and peripheral arteries among patients with various forms of ischemic heart disease

2019 ◽  
Vol 19 (2) ◽  
pp. 73-80
Author(s):  
Alexander R. Prudnikov
Keyword(s):  
Myocardial Infarction ◽  
Heart Disease ◽  
Coronary Arteries ◽  
Ultrasound Examination ◽  
Study Groups ◽  
Atherosclerotic Plaques ◽  
Syntax Score ◽  
Peripheral Arteries ◽  
Average Force ◽  
Atherosclerotic Lesions

The aim of the article. To determine the features of atherosclerotic lesions of the coronary and peripheral arteries in patients with various forms of coronary heart disease. Material and methods. Male patients with verified IHD diagnoses: stable angina pectoris of 2 FC and patients with myocardial infarction of different localization and severity were investigated. All of the examined patients were underwent ultrasound examination of peripheral arteries with assessment of vessel wall, intima-media complex and description of atherosclerotic plaques if they were presented in vessels. Results. The predominance of non-concentric atherosclerotic plaques of type 3 according to the classification of Gray-Weal and Geroulakos in peripheral arteries is noted. It was found that atherosclerotic plaques in the carotid arteries, combined with the thickening of the intima-media complex were more common in the group of patients with myocardial infarction. The amount of Syntax score I points, reflecting the severity of atherosclerotic lesions of the coronary arteries, did not differ significantly in the studied groups. The presence of direct correlation relationships of average force (p < 0,05) between the parameters of peripheral artery atherosclerosis severity and Syntax score I points, as well as the number of affected coronary arteries in the study groups was noted. Conclusion. The results indicate a close relationship between carotid and coronary atherosclerosis, which determines the importance of using ultrasound examination of peripheral arteries (in particular, brachiocephalic) to assess the risk of recurrent acute coronary events.

scholarly journals Relationship between the Activity of Matrix Metalloproteinase-2 and -9 in Myocardial Homogenate with Changes of the Cells Composition in the Coronary Arteries Wall in the Experiment

2021 ◽  
Vol 6 (3) ◽  
pp. 128-134
Author(s):  
N. S. Tryasak ◽  
◽  
Yu. V. Kozlova
Keyword(s):  
Extracellular Matrix ◽  
Matrix Metalloproteinase ◽  
Coronary Arteries ◽  
Matrix Metalloproteinase 9 ◽  
Matrix Metalloproteinase 2 ◽  
Atherosclerotic Lesions ◽  
Extracellular Matrix Components ◽  
Incomplete Freund’S Adjuvant ◽  
Matrix Components ◽  
Metalloproteinase 9

Matrix metalloproteinases are involved in a complex multifactorial process of atherosclerotic plaque formation and play a leading role in the degradation of the extracellular matrix components and increase the migratory activity of cellular elements of the vascular wall. Despite a number of scientific studies, it is necessary to identify clear biochemical markers for the development of atherosclerotic lesions. The purpose of the study was to investigate the relationship between the activity of matrix metalloproteinase-2 and matrix metalloproteinase-9 in myocardial homogenate with changes of the cells composition in the coronary arteries wall in experimental atherosclerosis. Materials and methods. The studies were performed on 76 nonlinear rats, which were divided into 3 groups: group Ia was the control (n=20) – animals, injected intracutaneously with 0.1 ml of 0.9 % sodium chloride solution; Ib – comparison group (n=20) – animals injected with incomplete Freund’s adjuvant at the dose of 0.1 ml intracutaneously and II – experimental group (n=36), which were immunized with native human low-density lipoprotein at a single dose of 200 μg, diluted in 0.1 ml of incomplete Freund’s adjuvant, regardless of the weight. The experiment lasted for 20 weeks. Material sampling was performed, starting from the 4th week after the drug administration. From the coronary arteries and the adjacent myocardium, microslides were made according to the generally accepted technique, which were stained with hematoxylin and eosin, according to the methods of Van Gizon, Mallory and Sudan III. The activity of matrix metalloproteinase-2 and matrix metalloproteinase-9 was determined by enzyme-zimografic method. Results and discussion. The growth of matrix metalloproteinase-2 and matrix metalloproteinase-9 activity in atherosclerotic lesions showed stages of degradation of extracellular matrix components: the dynamics of matrix metalloproteinase-2 activity during the experiment increased from 109.1±1.23 % at the 12th week to 127.32±0.99 % at the 20th week. The increased activity of matrix metalloproteinase-2 was associated with an increase in the number of leukocytes and macrophages, including foam cells. The activity of matrix metalloproteinase-9 reached the highest values of 98.24±0.82% at the 8th period from the onset of changes to the final level of 86.26±0.54% at the maximum terms of the experiment. Conclusion. The growing activity of matrix metalloproteinase-9 indicated the development of early atherosclerotic lesions, while the high level of activity of matrix metalloproteinase-2 indicated significant structural changes in the wall of the coronary arteries

Characteristic of apoptosis of coronary artery cells with atherosclerotic lesions

2016 ◽  
Vol 94 (9) ◽  
pp. 672-677
Author(s):  
Tatyana E. Vladimirskaya ◽  
I. A. Shved
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
Muscle Cells ◽  
Atherosclerosis Progression ◽  
Neointimal Thickness ◽  
Atherosclerotic Lesions ◽  
Atherosclerotic Process ◽  
Histopathological Studies

Aim. To study apoptosis of endothelial cells (EC), macrophages (MF) and smooth muscle cells (SMC) in the early atherosclerotic process (prior to plaque formation), elucidate mechanisms of its realization and evaluate effect on progression of atherosclerosis. Materials and methods. Histopathological studies were performed on coronary arteries affected by atherosclerosis takenat autopsy of patients with coronary heart disease (n = 63). To detect apoptosis, the TUNEL method was used for calculating the apoptotic index (AI) in paraffin sections. Phenotyping the cells and test for expression of active caspase 3 (AC-3) and apoptosis-inducing factor (AIF) were performed using sections of coronary arteries stained by immunohistochemistry. Results. The study of apoptosis showed a significant (p <0.0001) increase in AI of SMC, EC, MF coronary arteries affected by atherosclerosis compared with unaffected vessels. Progression of the atherosclerotic process led to a decrease of AI of SMC and EC. Statistical analysis revealed moderate feedback between AI of SMC and neointimal thickness in the development of atherosclerotic lesions (r = -0,44, p <0.0001). The amount of the AC-positive SMC and EC at the stage of lipoidosis significantly (p <0.0001) exceeded the number of AC -positive SMC at the liposclerosis stage. Expression of AIF was observed in the nuclei of EC in the newly formed vessels of hyperplastic intima. Conclusions. Early atherosclerotic lesions of the coronary arteries are accompanied by intense apoptosis of SMC, EC and MF. The intensity of apoptosis of SMC and EC decreases with the development of atherosclerosis. Progression of intimal hyperplasia at the early stages of atherosclerosis is associated with reduced apoptosis of smooth muscle cells and enhanced macrophage apoptosis. Apoptosis of SMC and MF is caspase-dependent. Apoptosis of endothelial cells can occur both with the participation of caspases and independently of them (with AIF).

Effect of Lipoprotein(a) and LDL on Plasminogen Binding to Extracellular Matrix and on Matrix-dependent Plasminogen Activation by Tissue Plasminogen Activator

1996 ◽  
Vol 75 (03) ◽  
pp. 497-502 ◽  
Author(s):  
Hadewijch L M Pekelharing ◽  
Henne A Kleinveld ◽  
Pieter F C.C.M Duif ◽  
Bonno N Bouma ◽  
Herman J M van Rijn
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Binding Sites ◽  
Umbilical Vein ◽  
Single Step ◽  
Plasminogen Activation ◽  
Structural Homology ◽  
Tissue Plasminogen ◽  
Umbilical Vein Endothelial Cells

SummaryLp(a) is an LDL-like lipoprotein plus an additional apolipoprotein apo(a). Based on the structural homology of apo(a) with plasminogen, it is hypothesized that Lp(a) interferes with fibrinolysis. Extracellular matrix (ECM) produced by human umbilical vein endothelial cells was used to study the effect of Lp(a) and LDL on plasminogen binding and activation. Both lipoproteins were isolated from the same plasma in a single step. Plasminogen bound to ECM via its lysine binding sites. Lp(a) as well as LDL were capable of competing with plasminogen binding. The degree of inhibition was dependent on the lipoprotein donor as well as the ECM donor. When Lp(a) and LDL obtained from one donor were compared, Lp(a) was always a much more potent competitor. The effect of both lipoproteins on plasminogen binding was reflected in their effect on plasminogen activation. It is speculated that Lp(a) interacts with ECM via its LDL-like lipoprotein moiety as well as via its apo(a) moiety.

Neutrophil Derived Cathepsin G Induces Potentially Thrombogenic Changes in Human Endothelial Cells: a Scanning Electron Microscopy Study in Static and Dynamic Conditions

1994 ◽  
Vol 72 (01) ◽  
pp. 140-145 ◽  
Author(s):  
Valeri Kolpakov ◽  
Maria Cristina D'Adamo ◽  
Lorena Salvatore ◽  
Concetta Amore ◽  
Alexander Mironov ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Thrombus Formation ◽  
Cathepsin G ◽  
Arterial Segment ◽  
Dynamic Conditions ◽  
Activated Neutrophils ◽  
Scanning Electron

SummaryActivated neutrophils may promote thrombus formation by releasing proteases which may activate platelets, impair the fibrinolytic balance and injure the endothelial monolayer.We have investigated the morphological correlates of damage induced by activated neutrophils on the vascular wall, in particular the vascular injury induced by released cathepsin G in both static and dynamic conditions.Human umbilical vein endothelial cells were studied both in a cell culture system and in a model of perfused umbilical veins. At scanning electron microscopy, progressive alterations of the cell monolayer resulted in cell contraction, disruption of the intercellular contacts, formation of gaps and cell detachment.Contraction was associated with shape change of the endothelial cells, that appeared star-like, while the underlying extracellular matrix, a potentially thrombogenic surface, was exposed. Comparable cellular response was observed in an “in vivo” model of perfused rat arterial segment. Interestingly, cathepsin G was active at lower concentrations in perfused vessels than in culture systems. Restoration of blood flow in the arterial segment previously damaged by cathepsin G caused adhesion and spreading of platelets on the surface of the exposed extracellular matrix. The subsequent deposition of a fibrin network among adherent platelets, could be at least partially ascribed to the inhibition by cathepsin G of the vascular fibrinolytic potential.This study supports the suggestion that the release of cathepsin G by activated neutrophils, f.i. during inflammation, may contribute to thrombus formation by inducing extensive vascular damage.

Perturbation of Platelet Adhesion to Endothelial Cells by Plasminogen Activation In Vitro

1997 ◽  
Vol 78 (02) ◽  
pp. 934-938 ◽  
Author(s):  
Hsiun-ing Chen ◽  
Yueh-I Wu ◽  
Yu-Lun Hsieh ◽  
Guey-Yueh Shi ◽  
Meei-Jyh Jiang ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Platelet Adhesion ◽  
Treatment Time ◽  
Shape Change ◽  
Umbilical Vein ◽  
Tissue Type ◽  
Apical Surface ◽  
Plasminogen Activation

SummaryTo investigate whether the endothelium-platelet interactions may be altered by plasminogen activation, cultured human umbilical vein endothelial cells (ECs) were treated with tissue-type plasminogen activator (t-PA) in the presence of plasminogen, and platelet adhesion to ECs was subsequently measured by using a tapered flow chamber. Our results demonstrated that platelets adhered more readily to t-PA treated EC monolayer than to the control monolayer at all shear stress levels tested. This phenomenon was treatment time-dependent and dose-dependent, and it could be blocked by adding plasmin inhibitors, such as e-amino caproic acid and aprotinin. Adherent platelets on t-PA treated EC monolayer underwent more severe shape change than those on the control monolayer. While the extracellular matrix directly treated with t-PA attracted less platelets than the control matrix did, platelet adhesion to the matrix that was produced by t-PA-treated ECs was unaltered. These data suggest that t-PA treatment on ECs compromised antiplatelet-adhesion capability on their apical surface without altering the reactivity of their extracellular matrix towards platelets.

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