Function of s100 Protein in Coronary Atherosclerosis

Atherosclerosis is a complex disease whose pathogenesis includes endothelial activation, accumulation of lipids in the subendothelium, formation foam cells, fat bands and atherosclerotic plaque. These mechanisms involve different cell populations intimate sub-endothelium, S-100 protein family plays role number extracellular intracellular processes during development lesions. The aim this study was to determine phenotypic characteristics smooth muscle cells consequent expression S100 altered coronary arteries advanced stages atherosclerosis. 19 samples right fibro atheroma (type V lesion) complicated lesions VI have been analyzed. According standard protocol, following primary antibodies used immunohistochemical analysis: a-smooth actin (α-SMA), vimentin protein. All analyzed atherosclerosis, (stage lesions) lesions). Most them had structure lesion with or as basis, subsequently by disruption (subtype a), hemorrhage b) thrombosis c), well presence several complications on same sample. Marked hypocellularity present subendothelium plaques. Cell population at plaque margins characterized immunoreactivity α-SMA, vimentin, Some these accumulate look like cells. In plaques, synthetic phenotype are present, some which demonstrate immunoreactivity. Summarizing numerous literature data our results, we could assume that due their proliferative activity earlier pathogenesis, protein, atherosclerosis which, study, result origin