**6. Stellate cells and atherosclerosis-related manifestations**

Is there any relationship between changes in cellular composition and the well-known manifestations of atherosclerosis such as intimal thickening and accumulation of lipids and collagen? The strongest correlation was established between the number of stellate cells, on the one hand, and the content of cholesteryl esters and total lipids, on the other [14]. The correlation coefficients between the number of stellate cells and collagen content and intimal thickness were somewhat lower; nevertheless, they remained greater than the correlation coefficients for elongated cells and the total cell content [14].

Stellate cells are located in the close proximity to endothelial lining; they are the first barrier for the compounds entering the vascular wall from the blood. This may account for the great extent of the involvement of the stellate cells in atherosclerotic manifestations in the vascular wall [1, 14].

The direct correlation between the number of stellate cells and atherosclerotic manifestations raised a number of questions. Why do cells become stellate? Are stellate cells specific to cell type or does this shape reflect the functional state of a cell? In the human body, there are other tissues containing stellate cells, for example, neurons and other nervous cells, dendritic cells of lymphatic follicles, Ito cells in the liver, mesangial cells in renal glomeruli, etc. [1]. These cells serve predominantly communicative functions via a system of their processes [1]. A similar function can be ascribed to stellate cells of subendothelial intima, which form an integrating communication network by their long branching processes [1].

In primary cultures, intimal cells are generally flattened and polygonal. In these cell cultures, arborization, i.e., formation of stellate cells, using cAMP elevators, was induced [12]. Almost all cells derived from the proteoglycan-rich layer become stellate, while the content of stellate cells is not higher than 50% in cultures from the muscular-elastic layer and about 10% in cultures from the media [12].

Arborization is accompanied by redistribution of connexin 43 (Cx43), a major protein of specific cell-to-cell contacts (gap junctions). This protein is localized on cell surface in specific structures, so-called Cx43 plaques. On nonarborized cells, small Cx43 plaques are unevenly distributed over the cell surface. In addition to small Cx43 plaques, on arborized (stellate) cells, large Cx43 plaques are localized predominantly on the ends of the cellular processes in the areas of the cell-to-cell contacts [12].

Thus, an increase in the intracellular cAMP content leads to arborization of subendothelial intima cells. Changes in the cell shape are accompanied by redistribution of connexin 43 plaques and, probably, by increase of the rate of the intercellular communication via gap junctions. This suggests that the stellate shape is important for the formation of cell-to-cell contacts in the intima. Subendothelial intimal cells differ from medial smooth muscle cells, which are poorly or not arborized, by the ability to form these contacts. Therefore, it is reasonable to suggest that subendothelial intimal cells are a specific cell type distinct from typical smooth muscle cells.
