THE CELL-ADHESION MOLECULE E-CADHERIN IS WIDELY EXPRESSED IN HUMAN ATHEROSCLEROTIC LESIONS

Citation
Yv. Bobryshev et al., THE CELL-ADHESION MOLECULE E-CADHERIN IS WIDELY EXPRESSED IN HUMAN ATHEROSCLEROTIC LESIONS, Cardiovascular Research, 40(1), 1998, pp. 191-205
Citations number
40
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00086363
Volume
40
Issue
1
Year of publication
1998
Pages
191 - 205
Database
ISI
SICI code
0008-6363(1998)40:1<191:TCMEIW>2.0.ZU;2-N
Abstract
Objective: Various cell adhesion molecules are expressed in atherogene sis and the significance of their involvement in atherosclerotic lesio n formation is well appreciated, in the present work, we examined whet her the Ca2+-dependent cell adhesion molecule E-cadherin is also invol ved in atherogenesis. Methods: Specimens of carotid artery and aorta w ere 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 a lso applied to examine how the accumulation of oxidised low density li poproteins (LDL) by intimal cells is associated with E-cadherin expres sion. Results: No E-cadherin(+) cells were found in normal non-atheros clerotic intima but E-cadherin(+) cells were present in 96% of the ath erosclerotic lesions. In atherosclerotic intima, E-cadherin was expres sed by intimal cells showing varying degrees of transformation into fo am cells. These E-cadherin+ cells also contained oxidised LDL in their cytoplasm. Differing numbers of CD68(+) foam cells (15% to 60%) expre ssed E-cadherin but all the CD68(+) macrophages without signs of trans formation into foam cells were negative for E-cadherin. Neither smooth muscle cells nor foam cells of smooth muscle cell origin (smooth musc le alpha-actin(+)) were found to be positive for E-cadherin. T-cells ( CD3(+)) and endothelial cells (von Willebrand factor(+)) were also neg ative for E-cadherin. Only a few vascular dendritic cells (S-100(+)) e xpressed E-cadherin and their expression was weak. We also found that a large proportion (40% to 85%) of E-cadherin(+) cells did not stain w ith any cell-type specific markers. Conclusions: The finding that E-ca dherin is expressed in atherosclerotic lesions expands our knowledge o f cell adhesion molecules involved in atherogenesis. That E-cadherin i s expressed in intimal cells transforming into foam cells suggests tha t lipid accumulation might be associated with the alteration and reorg anisation of cell-to-cell interactions in atherogenesis. The present o bservations might assist in understanding the mechanisms associated wi th intracellular lipid accumulation. (C) 1998 Elsevier Science B.V. Al l rights reserved.