Interaction of Vascular Smooth Muscle Cells and Endothelial Cells in Atherosclerosis on the Background of Metabolic Syndrome
Authors: Mankovskyi Dmytro , Chuiko Nataliia 
Published: February 2024

The objective: was to determine the interaction of vascular smooth muscle cells with endothelial cells in the process of atherogenesis in the presence of metabolic syndrome.
Materials and methods. We studied the following groups: Group I – 50 patients who died as a result of complications associated with cerebral atherosclerosis in the setting of metabolic syndrome, Group II – 50 patients who died as a result of complications associated with cerebral atherosclerosis without a history metabolic syndrome and Group III (comparison group) – 50 patients who died from causes unrelated to MS and AS.
For the study we used the following histological and histochemical methods: hematoxylin-eosin, Masson’s method, Van Gieson’s method, Weigert’s method, and immunohistochemical examination using monoclonal antibodies. For the identification of smooth muscle cells: immunocytochemical markers – Actin Smooth Muscle Ab-1 (Clone 1A4), Vimentin Ab-2 (Clone V9), Desmin (Muscle Cell Marker Ab-1 Clone D33), immunocompetent cells – CD4 (CD4 Ab-8), CD8 (SP-16), CD20 (CD20 Ab-1), CD68 (CD68/Macrophage Marker Ab-4) and to determine the endothelium state, immunocytochemical marker – CD31/PECAM-1 (Endothelial Cell Marker) Ab-1.
Results. In atherosclerotic lesions of cerebral arteries with metabolic syndrome manifestations, in the arterial wall media a significantly higher expression of desmin was observed in smooth muscle cells (SMCs) compared to other study groups. It should be noted that the migration of smooth muscle cells from the media and their intensive proliferation is directly dependent on endothelial and fibroblast factors. The immunohistochemical reaction with vimentin revealed the presence of connective tissue components and severe arterial wall fibrosis.
The expression of vimentin showed that vascular wall fibrosis increases with the progression of the underlying disease – metabolic syndrome. We observed migration and proliferation of SMCs, endocytosis, and synthesis of connective tissue components that actively contribute to intimae hypertrophy and atheromatous changes. As for the change in VSMCs phenotype, they demonstrate an extremely high degree of plasticity, and this affects the loss of expression of their contractile genes, including smooth muscle cell alpha-actin. We also noted potentiation of atherosclerotic changes resulted from formation of less differentiated forms of smooth muscle cells.
Atherogenesis can be initiated by both certain substances, such as cholesterol and lipoproteins, and endothelial changes – activated and damaged endothelium can participate in atherogenesis. Endothelial activation is also accompanied by the production of cell growth factors (Sitia S. Et al., 2010). We observed monocyte adhesion to the arterial endothelium, the presence of monocytes under the endothelium their migration into the intimae with subsequent proliferation and formation of foam cells. This indicates their important role in the development of atherosclerosis by potentiating inflammation in the vascular wall and promoting the VSMCs phenotype transformation.
Conclusions. Changes in the phenotype of arterial intimae SMCs are accompanied by increased proliferation, and modified SMCs, with their high activity of synthesis of extracellular connective tissue components (elastin, collagen and glycosaminoglycans), are responsible for the formation of the plaques fibrous base. The presence of lymphocytes in the atherosclerotic process involves interaction with macrophages, endothelial cells and SMCs. A decrease in the number of endothelial progenitor cells, which are actively involved in the process of endothelial regeneration, contributes to the development of atherosclerosis.