Actin, tropomyosin and peroxiredoxin-2 in atherosclerotic plaques at different stages of development in coronary atherosclerosis

2021 ◽  
Vol 331 ◽  
pp. e102
Author(s):  
E.M. Stakhneva ◽  
I.A. Meshcheryakova ◽  
E.A. Demidov ◽  
K.V. Starostin ◽  
S.E. Peltek ◽  
...  
2020 ◽  
Vol 315 ◽  
pp. e113
Author(s):  
E. Stakhneva ◽  
I. Meshcheryakova ◽  
E. Demidov ◽  
K. Starostin ◽  
S. Peltek ◽  
...  

Diagnostics ◽  
2019 ◽  
Vol 9 (4) ◽  
pp. 177 ◽  
Author(s):  
Ekaterina M. Stakhneva ◽  
Irina A. Meshcheryakova ◽  
Evgeny A. Demidov ◽  
Konstantin V. Starostin ◽  
Evgeny V. Sadovski ◽  
...  

Background: To study the changes in protein composition of atherosclerotic plaques at different stages of their development in coronary atherosclerosis using proteomics. Methods: The object of research consisted of homogenates of atherosclerotic plaques from coronary arteries at different stages of development, obtained from 15 patients. Plaque proteins were separated by two-dimensional electrophoresis. The resultant protein spots were identified by the matrix-assisted laser desorption ionization method with peptide mass mapping. Results: Groups of differentially expressed proteins, in which the amounts of proteins differed more than twofold (p < 0.05), were identified in pools of homogenates of atherosclerotic plaques at three stages of development. The amounts of the following proteins were increased in stable atherosclerotic plaques at the stage of lipidosis and fibrosis: vimentin, tropomyosin β-chain, actin, keratin, tubulin β-chain, microfibril-associated glycoprotein 4, serum amyloid P-component, and annexin 5. In plaques at the stage of fibrosis and calcification, the amounts of mimecan and fibrinogen were increased. In unstable atherosclerotic plaque of the necrotic–dystrophic type, the amounts of human serum albumin, mimecan, fibrinogen, serum amyloid P-component and annexin were increased. Conclusion: This proteomic study identifies the proteins present in atherosclerotic plaques of coronary arteries by comparing their proteomes at three different stages of plaque development during coronary atherosclerosis.


2019 ◽  
Vol 287 ◽  
pp. e278
Author(s):  
E. Kashtanova ◽  
Y. Polonskaya ◽  
E. Stakhneva ◽  
A. Kurguzov ◽  
I. Murashov ◽  
...  

2019 ◽  
Vol 287 ◽  
pp. e163
Author(s):  
V. Shramko ◽  
Y. Ragino ◽  
E. Kashtanova ◽  
Y. Polonskaya ◽  
S. Morozov ◽  
...  

Author(s):  
E. V. Shakhtshneider ◽  
D. E. Ivanoshchuk ◽  
Yu. I. Ragino ◽  
V. S. Fishman ◽  
Ya. V. Polonskaya ◽  
...  

Aim. The goal of the study was to analyze the differential expression of lipid metabolism-related genes in the atherosclerotic plaques of different types in patients with coronary atherosclerosis.Material and Methods. The study was performed on the specimens of atherosclerotic plaques in 45–65-year-old patients with coronary atherosclerosis with stable exertional angina functional class II-IV without acute coronary syndrome. Coronary atherosclerosis was verified by coronary angiography. Atherosclerotic plaque tissue was sampled intraoperatively when indicated. Whole-genome sequencing of ribonucleic acid (RNA) was performed using the TruSeq RNA Sample Preparation Kit (Illumina, USA).Results. We analyzed the differences in the expression of 12 genes including LDLR, APOB, PCSK9, LDLRAP1, LIPA, STAP1, ABCA1, APOA1, APOE, LPL, SCARB1, and SREBF2 depending on the type of atherosclerotic plaques. The expression level of APOE gene was eight times higher in unstable atherosclerotic plaques of dystrophic-necrotic type (p < 0.0001). The expression levels of LDLR and APOB genes were eight times higher in stable atherosclerotic plaques (p < 0.0001). We did not find differences in the expression levels of the ABCG5, ABCG8, APOC3, CETP, CLPS, CYP7A1, and PNPLA5 genes.Conclusion. The study showed the differences in the activity of individual metabolism-related genes in the atherosclerotic plaques of different types in patients with coronary atherosclerosis. Obtained data may become the basis for the development of test systems aimed at predicting the development of atherosclerotic process and its complications.


Author(s):  
Frank Gijsen ◽  
Anna Ten Have ◽  
Jolanda Wentzel ◽  
Antonius Van Der Steen

Ischaemic heart disease is most frequently caused by coronary atherosclerosis, of which the vulnerable plaque is one of the developmental stages. Rupture of a vulnerable plaque with superimposed thrombosis frequently leads to acute coronary syndromes. The major components of a vulnerable plaque are a lipid-rich, atheromatous core, and a thin fibrous cap with macrophage and macrophage infiltration (Schaar et al., 2004). After the first paper suggesting the possibility of thermographic detection of vulnerable plaques (Casscells et al., 1996), intracoronary thermography as a vulnerable plaque detection technique has been investigated. Increased metabolic activity of macrophages is suggested as the main reasons for the increased temperatures (ten Have et al., 2005).


2018 ◽  
Vol 33 (3) ◽  
pp. 93-101 ◽  
Author(s):  
E. I. Yaroslavskaya ◽  
V. A. Kuznetsov ◽  
E. A. Gorbatenko ◽  
S. M. Dyachkov

Evidence suggests that most myocardial infarctions result from ruptures of the atherosclerotic plaques that do not significantly compromise coronary lumen before the event. However, detection of nonsignificant coronary lesions in patients with suspected coronary artery disease without coronary angiography is challenging. We developed a calculator for nonobstructive coronary atherosclerosis based on patient gender, age, and the presence or absence of the echocardiographic signs of ascending aorta atherosclerosis and arterial hypertension. The calculator may be used for determining the probability of non-obstructive coronary atherosclerosis and for promoting compliance of patients to lipid-lowering therapy.


2021 ◽  
Vol 64 (2) ◽  
pp. 58-64
Author(s):  
Mihail Tasnic ◽  
◽  
Ilia Catereniuc ◽  

Background: Myocardial bridges are variants of the intramyocardial position of the coronary arteries. In the specialty literature, hot topics in cardiovascular field are myocardial infarction and non-obstructive coronary artery disease with frequent connection with myocardial bridges. Material and methods: The morphological study was based on the analysis of 200 human hearts and fragments of coronary arteries. The retrospective study was focused on the analysis of 6168 coronary angiography reports, to identify patients with myocardial bridges, their preferred location, the degree of systolic stenosis, the association between myocardial bridges and proximal to bridge and under the bridge coronary atherosclerosis. Results: The complete myocardial bridges were described in 62% of the analyzed hearts and only in 5.3% of the total number of studied coronarographies. In the majority of cases, the complete myocardial bridges covered the anterior interventricular branch. The degree of subpontine arterial systolic stenosis varied within 10-95%. The comparative study did not determine any correlations between the degree of subpontine vascular compression and the degree of the left ventricular myocardial hypertrophy. In 32% of cases were described proximal to bridge atherosclerotic plaques and only in one case (0.5%) – distal to bridge atherosclerotic plaques, located immediately under the bridge. Conclusions: The research findings underline the differences in anatomical and angiographic incidence of myocardial bridges, and the inability of all bridges to reduce the lumen of under bridged artery. Current study emphasizes attention to the topography of bridges, the correlation with ventricular hypertrophy and coronary atherosclerosis.


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