Белок S100A8 в атеросклеротических поражениях у человека

Abstract

Introduction. In the pathogenesis of atherosclerosis, a change in the content of different proteins in S100 protein family may play an important role in the formation of atherosclerotic lesions in the vascular wall. The aim was to study the content of mononuclear cells expressing protein S100A8 in different types of atherosclerotic lesions secondary to the development of the inflammatory process in the vascular wall during atherogenesis in humans. Materials and methods. Immunohistochemical and morphometric studies were performed on autopsy material (18 cases) obtained from patients who died from acute cardiovascular insufficiency of atherosclerotic etiology. We detected the expression of S100A8 protein in the aortic segments (from the arc, thoracic and abdominal regions), coronary arteries, and arteries of the circle of Willis (40 tissue samples) using a highly sensitive two-stage streptavidin-biotin method. Comparative analysis was subjected to normal areas of arteries, lipid stain, and unstable and stable atherosclerotic plaques. We performed a statistical analysis with the computer program Statistica Version 10. The significance of the differences between the samples studied was determined by the Student’s T-criterion. Results. Intracellular localization of S100A8 protein was found in the intima of unstable atherosclerotic lesions. Its expression was mainly concentrated in the cytoplasm of macrophages. Intracellular production of S100A8 was minimal or absent in normal areas of aorta intima, coronary arteries, a. basilaris, and in the cap of stable atherosclerotic plaques. We detected numerous inflammatory mononuclear cell infiltrates in the areas of the vascular wall with S100A8 expression. According to the morphometry, their content in the intima of unstable plaques significantly exceeded the similar rate in the intima of normal areas of arteries and stable lesions. Conclusion. We hypothesize that protein S100A8 may contribute to the activation of immune-inflammatory reactions in the vascular wall, which are the basis for the formation of unstable progressive atherosclerotic lesions leading to the development of acute coronary syndrome. Further research may provide more evidence to support that S100A8 proteins are a promising drug target in the prevention and therapy of atherosclerosis. Keywords: atherogenesis, S100A8 protein, unstable atherosclerotic plaque