Alterations in expression of surface adhesion molecules on resident vascula
r and blood-derived cells play a fundamental role in the pathogenesis of ca
rdiovascular disease. Smooth muscle cells (SMCs) have been shown to express
T-cadherin (T-cad). an unusual GPI-anchored member of the cadherin family
of adhesion molecules. Particular relevance for T-cad in cardiovascular tis
sues is indicated by our present screen (immunoblotting) of human tissues a
nd organs whereby highest expression of T-cad was found in aorta, carotid,
iliac and renal arteries and heart. To explore the (patho)physiological rol
e for T-cad in the vasculature we performed an immunohistochemical analysis
of T-cad expression in normal human aorta and atherosclerotic lesions of v
arying severity. T-cad was present both in the intima and media and was exp
ressed in endothelial cells (ECs), SMCs and pericytes, but not in monocytes
/macrophages, foam cells and lymphocytes. In the adventitia T-cad was prese
nt in the wall of vasa vasorum and was expressed in ECs, SMCs and pericytes
, T-cad was differentially expressed in SMCs from distinct vascular layers
of normal aorta (for example, high in the subendothelial (proteoglycan) lay
er of the intima, low in the musculoelastic intimal layer and in the media)
, as well as at different stages of lesion progression. In SMCs there was a
n apparent inverse relationship between the intensities of T-cad and smooth
muscle a-actin expression, this being most prominent in lesions. The findi
ngs suggest a phenotype-associated expression of T-cad which may be relevan
t to control of the normal vascular architecture and its remodelling during
atherogenesis.