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American Journal of Pathology, Vol 150, 509-521, Copyright © 1997 by American Society for Investigative Pathology
REGULAR ARTICLES |
P Neuville, A Geinoz, G Benzonana, M Redard, F Gabbiani, P Ropraz and G Gabbiani
Department of Pathology, University of Geneva CMU, Switzerland.
Previous work (M.-L. Bochaton-Piallat, P. Ropraz, F. Gabbiani, G. Gabbiani, Arterioscler Thromb Vasc Biol 1996, 16:815-820) has shown that a subset of smooth muscle cell (SMC) clones derived from the normal rat aortic media displays an epithelioid phenotype similar to that of the whole SMC population cultured from the intimal thickening 15 days after endothelial injury (IT-15). We show here that the whole IT-15 SMC population and the epithelioid clones, derived either from the normal media or from the IT-15, express cellular retinol-binding protein-1 (CRBP-1), a protein involved in retinoid metabolism. The expression of CRBP-1 is accompanied by the expression of cytokeratin 8. In both whole SMC population cultured from IT-15 and epithelioid clones, retinoic acid modulates the transition from the epithelioid phenotype to the spindle phenotype, typical of whole SMC populations cultured from the rat normal aortic media. Moreover, after endothelial injury in vivo, a CRBP-1 expressing SMC subset appears transiently in the IT and disappears, allegedly by apoptosis, when re- endothelialization takes place. Our results suggest that the expression of CRBP-1 is a marker of arterial SMC activation after endothelial injury in vivo and that CRBP-1 and probably retinoids participate in this process.
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