Myeloperoxidase and elastic-collagen frame in the formation of unstable atherosclerotic plaque in human
- 作者: Pigarevsky P.V.1, Maltseva S.V.1, Snegova V.A.1, Davydova N.G.1, Yakovleva O.G.1
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隶属关系:
- Institute of Experimental Medicine, St. Petersburg
- 栏目: Original Study Articles
- URL: https://cijournal.ru/1684-7849/article/view/636132
- DOI: https://doi.org/10.17816/CI636132
- ID: 636132
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详细
Background: Currently, there is a number of evidence indicating the possible involvement of myeloperoxidase in the pathogenesis of atherosclerosis. However, its role in the formation of unstable atherosclerotic lesions in human and its effect on the elastic-collagen frame in the vascular wall remain poorly studied.
AIM: The purpose of the work is to conduct a comparative immunohistochemical analysis of the content of myeloperoxidase, smooth muscle cells, as well as elastic and collagen fibers in various types of atherosclerotic lesions in human.
Materials and methods: Histological and immunohistochemical examination was carried out on autopsy material (21 cases) obtained from persons who died from acute cardiovascular failure of atherosclerotic etiology. The segments of the aorta (from the arch, thoracic and abdominal regions), coronary arteries and basilaris arteries were examined - a total of 50 tissue samples. Expression of myeloperoxidase in various types of atherosclerotic lesions of the vascular wall was detected by a highly sensitive two-step avidin-biotin method.
Results: Intracellular localization of myeloperoxidase was found in the intima of unstable atherosclerotic plaques, which increases as this type of atherosclerotic lesion progresses. At the same time, unstable plaques show a sharp decrease in the number of smooth muscle cells and destruction of the elastic-collagen frame with the destruction of elastic and collagen fibers and the rupture of the plaque cap.
Conclusion: It is hypothesized that the production of myeloperoxidase by mononuclear cells can have a negative effect on smooth muscle cells, promoting their apoptosis, followed by inhibition of the synthesis of elastic and collagen fibers in the vascular wall. Established facts can be considered as a mechanism leading to destabilization of atherosclerotic damage in human.
作者简介
Peter Pigarevsky
Institute of Experimental Medicine, St. Petersburg
Email: pigarevsky@mail.ru
ORCID iD: 0000-0002-5906-6771
SPIN 代码: 8636-4271
Dr. Sci. (Biol.), Head of the Laboratory of Atherosclerosis named after N.N. Anichkov, Department of Biochemistry
俄罗斯联邦, adress:12 Akad. Pavlov street, 197376, Saint Petersburg, RussiaSvetlana Maltseva
Institute of Experimental Medicine, St. Petersburg
Email: moon25@rambler.ru
ORCID iD: 0000-0001-7680-8485
SPIN 代码: 8367-9096
Cand. Sci. (Biology), Researcher Associate department of biochemistry
俄罗斯联邦, adress:12 Akad. Pavlov street, 197376, Saint Petersburg, RussiaVlada Snegova
Institute of Experimental Medicine, St. Petersburg
Email: biolaber@inbox.ru
ORCID iD: 0000-0002-9925-2886
SPIN 代码: 8088-4446
Cand. Sci. (Biology), Researcher Associate department of biochemistry
俄罗斯联邦, adress:12 Akad. Pavlov street, 197376, Saint Petersburg, RussiaNatalya Davydova
Institute of Experimental Medicine, St. Petersburg
Email: tatashaspb@yandex.ru
ORCID iD: 0000-0002-4522-6789
SPIN 代码: 4761-3575
Cand. Sci. (Medicine), Researcher Associate department of biochemistry
俄罗斯联邦, adress:12 Akad. Pavlov street, 197376, Saint Petersburg, RussiaOlga Yakovleva
Institute of Experimental Medicine, St. Petersburg
编辑信件的主要联系方式.
Email: emalonett@yandex.ru
ORCID iD: 0000-0002-6248-9468
SPIN 代码: 4963-5064
Researcher Associate department of biochemistry
俄罗斯联邦, adress:12 Akad. Pavlov street, 197376, Saint Petersburg, Russia参考
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