Lipogenic stromal cells as members of the foam-cell population in human atherosclerosis: Immunocytochemical and ultrastructural assessment of 6 cases.

To identify the nature of foam cells in atherosclerosis, carotid atherosclerotic plaques (CAPs) from six patients were studied. Hematoxylin-and-eosin, Congo Red and Oil Red O staining were used to study histopathologic alterations in CAPs. CD31, α-smooth-muscle actin (α-SMA), CD68, desmin and S100 were stained immunohistochemically. The ultrastructure of foam cells was analyzed by transmission electron microscopy (TEM). CAPs were shown to be composed of a fibrous cap covering a dome-shaped mass with a peripheral, circumferential fringe merging with a basal band which itself met the tunica media, the latter consisting of smooth-muscle cells (SMCs). The interior of the dome-shaped mass exhibited fibrosis, neovascularization, hemorrhage, necrosis and calcification. Lipid droplets identified by histological stains and TEM were found in the rounded epithelioid foam cells regarded as macrophages, as well as in spindled cells interpreted here as lipoleiomyocytes (lipid-containing SMCs), lipofibroblasts and lipomyofibroblasts; and all these cells were located in different regions of the CAPs. All of these lipid-laden cells were strongly positive for CD68 but negative for desmin. Foam cells were weakly positive for α-SMA, CD31 and S100. The results indicate that the light microscopically identifiable population of foam/lipid-laden cells hide a spectrum of diverse differentiation ranging from the expected macrophage phenotype to non-macrophage phenotypes. The origin of these diverse cell phenotypes in terms of multipotential mesenchymal precursors and the origin of the intracellular lipid are discussed.

Histopathological and ultrastructural study of carotid atherosclerotic plaques: a study of four cases.

To clarify the characteristics and origin of the cellular components in atherosclerosis, carotid atherosclerotic plaques (CAPs) of four patients were studied by light microscopy using hematoxylin-eosin, Congo red and alpha-smooth-muscle actin stains, and by transmission electron microscopy of different regions of CAPs. By light microscopy, CAPs were composed of 1) a fibrous cap; 2) an atherosclerotic core presenting focal fibrosis, neovascularization, hemorrhage, necrosis, chondrification and ossification; and 3) a basal band composed of a hyperplasic pseudo-media and affected tunica media. Ultrastructurally, the CAPs contained a diversity of cells including fibroblasts, myofibroblasts, osteochondrocytes, vascular smooth-muscle cells, foam cells and other myoid cells characterized by varied features of the above mentioned cells. The results indicated that CAPs were derived from a proliferation of multipotential mesenchymal stem cells, leading to the presence of degenerated foam cells and lipid-laden cells.

A review: Pathological and molecular biological study on atherosclerosis.

Atherosclerosis is a disease in which the arterial intima thickens and transforms into a sclerotic plaque, interfering with normal blood flow and potentially leading to stroke or death. It is divided into three stages: the pre-stage, which is characterized by diffuse intimal thickenings (DITs) and fatty streaks, the early atherosclerotic stage, which is characterized by pathological intimal thickening (PIT), and the late stage, which is characterized by fibroatheromas transformed from PIT. Each stage of atherosclerosis is distinguished by distinct morphological changes, biological changes, and the expression of immune markers at various levels. This review summarizes discoveries and achievements in microanatomy, ultrastructure, immunohistochemical staining, and molecular biology in the literature on atherosclerosis. Based on our research, we have emphasized common histological changes and pathological mechanisms of atherosclerosis in this review.