The cell adhesion molecule E-cadherin is widely expressed in human atherosclerotic lesions

Objective: Various cell adhesion molecules are expressed in atherogenesis and the significance of their involvement in atherosclerotic lesion formation is well appreciated, in the present work, we examined whether the Ca2+-dependent cell adhesion molecule E-cadherin is also involved in atherogenesis. Methods: Specimens of carotid artery and aorta were obtained at operation. Expression of E-cadherin was studied by an immunohistochemical method. The nature of E-cadherin-expressing cells was examined by comparative analysis of consecutive sections and by a double immunostaining procedure. An immunohistochemical approach was also applied to examine how the accumulation of oxidised low density lipoproteins (LDL) by intimal cells is associated with E-cadherin expression. Results: No E-cadherin(+) cells were found in normal non-atherosclerotic intima but E-cadherin(+) cells were present in 96% of the atherosclerotic lesions. In atherosclerotic intima, E-cadherin was expressed by intimal cells showing varying degrees of transformation into foam cells. These E-cadherin+ cells also contained oxidised LDL in their cytoplasm. Differing numbers of CD68(+) foam cells (15% to 60%) expressed E-cadherin but all the CD68(+) macrophages without signs of transformation into foam cells were negative for E-cadherin. Neither smooth muscle cells nor foam cells of smooth muscle cell origin (smooth muscle alpha-actin(+)) were found to be positive for E-cadherin. T-cells (CD3(+)) and endothelial cells (von Willebrand factor(+)) were also negative for E-cadherin. Only a few vascular dendritic cells (S-100(+)) expressed E-cadherin and their expression was weak. We also found that a large proportion (40% to 85%) of E-cadherin(+) cells did not stain with any cell-type specific markers. Conclusions: The finding that E-cadherin is expressed in atherosclerotic lesions expands our knowledge of cell adhesion molecules involved in atherogenesis. That E-cadherin is expressed in intimal cells transforming into foam cells suggests that lipid accumulation might be associated with the alteration and reorganisation of cell-to-cell interactions in atherogenesis. The present observations might assist in understanding the mechanisms associated with intracellular lipid accumulation. (C) 1998 Elsevier Science B.V. All rights reserved.