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American Journal of Pathology, Vol 146, 1059-1064, Copyright © 1995 by American Society for Investigative Pathology
REGULAR ARTICLES |
ML Bochaton-Piallat, F Gabbiani, M Redard, A Desmouliere and G Gabbiani
Department of Pathology, University of Geneva, Switzerland.
Intimal thickening induced after endothelial denudation of rat aorta is though to be due to migration and proliferation of smooth muscle cells (SMC). When the reendothelialization is achieved, intimal thickening shows an important decrease in cellularity. Using in situ end labeling of fragmented DNA and electron microscopy, we show that this remodeling is accompanied by apoptosis of SMC. The number of apoptotic SMC becomes important 15 days after endothelial injury and reaches a maximum at 20 days; at 45 days the intimal thickening is reendothelialized and no more apoptotic SMC are detected. Apoptotic SMC show nuclear and cytoplasmic condensation as well as cytoplasmic vacuolization. Our results indicate that apoptosis is an important mechanism in the regulation of intimal thickening evolution.
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