Molecular analysis of arterial stenosis in rat carotids

Citation
A. Forte et al., Molecular analysis of arterial stenosis in rat carotids, J CELL PHYS, 186(2), 2001, pp. 307-313
Citations number
38
Categorie Soggetti
Cell & Developmental Biology
Journal title
JOURNAL OF CELLULAR PHYSIOLOGY
ISSN journal
00219541 → ACNP
Volume
186
Issue
2
Year of publication
2001
Pages
307 - 313
Database
ISI
SICI code
0021-9541(200102)186:2<307:MAOASI>2.0.ZU;2-B
Abstract
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.