A new model of surgical injury for the induction and development of stenosi
s in common rat carotids is described. This model differs from balloon angi
oplasty or vein graft systems currently applied on animals to develop steno
sis, since it involves the entire vessel wall layers and mimics the injury
occurring during arterial grafts, endarterectomy or organ transplantation.
At different times following arterial damage, the pattern of expression of
genes already known to be involved in the proliferation, differentiation, a
nd apoptosis of smooth muscle cells (c-myc, Angiotensin II receptor 1, Bcl-
2 and Bax alpha), as well as of Rb and Rb2 genes, whose pattern of expressi
on after arterial injury has not yet been reported, was analyzed by semi-qu
antitative reverse transcription-polymerase chain reaction technique. Histo
logical and histochemical analysis on carotid sections shows the morphologi
cal changes which occurred 30 days after surgical injury in the vessel wall
. Molecular and histological data demonstrate that this model of surgical i
njury induces neointimal proliferation in about 30% of rats. In about 70% o
f the remaining rats, it induces the processes responsible for negative rem
odelling, namely the significant accumulation of extracellular matrix and f
ibers and disorganization of arterial tunics. This model is therefore avail
able for further studies on the expression of genes involved in the arteria
l stenotic process, as wet as for testing drugs aimed at limiting this recu
rrent pathophysiological phenomenon. J. Cell. Physiol. 186:307-313, 2001. (
C) 2001 Wiley-Liss, Inc.