The arterial tenascin C expression in vivo and in vitro has been studi
ed using immunohistochemistry. The functional relevance of localized t
enascin C expression was assessed in vitro using various human cell ty
pes involved in the progression of vascular disease. Normotensive and
hypertensive rats exhibited age-dependent patterns of vascular (aorta)
tenascin expression, but the lumen-to-media-directed progression of t
enascin induction was accelerated in hypertensive rats, Tenascin-rich
neointimal lesions (spontaneous) were observed at branching sites of a
orta from aged (80 weeks) hypertensive rats. Subendothelial tenascin f
oci contained lipid-laden smooth muscle cells and monocytes/macrophage
s. Medial tenascin foci encaged smooth muscle cells which synthesized
DNA. Tenascin was expressed both in vivo and in vitro by endothelial a
nd smooth muscle cells but not by monocytes/macrophages; angiotensin I
I, oxidized-low density lipoprotein and transforming growth factor pi
induced expression of tenascin transcripts and glycoprotein in vitro.
Endothelial and smooth muscle cells, but not monocytes, adhered to ten
ascin substrata, Tenascin reduced focal adhesion integrity in confluen
t endothelial and smooth muscle cell cultures, Angiotensin II-induced
migration of endothelial and smooth muscle cells was accompanied by te
nascin deposition within extracellular matrix migration trails, Tenasc
in may function both as a defense against monocyte invasion and medial
smooth muscle replication, as well as a substratum for directed endot
helial and smooth muscle cell migration.