SMOOTH-MUSCLE CELL-PROLIFERATION, ELASTIN FORMATION, AND TROPOELASTINTRANSCRIPTS DURING THE DEVELOPMENT OF INTIMAL THICKENING IN RABBIT CAROTID ARTERIES AFTER ENDOTHELIAL DENUDATION
M. Aoyagi et al., SMOOTH-MUSCLE CELL-PROLIFERATION, ELASTIN FORMATION, AND TROPOELASTINTRANSCRIPTS DURING THE DEVELOPMENT OF INTIMAL THICKENING IN RABBIT CAROTID ARTERIES AFTER ENDOTHELIAL DENUDATION, HISTOCHEM C, 107(1), 1997, pp. 11-17
Extracellular matrix formation and smooth muscle cell proliferation ar
e two major factors contributing to the development of intimal thicken
ing after arterial injury. We investigated the elastin formation, trop
oelastin transcripts, and proliferation of smooth muscle cells during
the development of intimal thickening in rabbit carotid arteries after
balloon endothelial denudation. Tropoelastin transcripts, identified
by in situ hybridization using a digoxigenin-labeled probe, and elasti
n staining in the thickened intima were minimal 1 week after endotheli
al denudation when smooth muscle cell proliferation appeared throughou
t the thickened intima. A strong signal for tropoelastin transcripts w
as seen in the basal layer of the thickened intima 2 weeks after endot
helial denudation, and then in the surface layer of the thickened inti
ma 4 weeks after endothelial denudation. Immunohistochemistry for prol
iferating cell nuclear antigen and Ki-67, both markers for proliferati
ng cell nuclei, showed that tropoelastin transcripts and elastin forma
tion increased when smooth muscle cells enter quiescence after the end
of the proliferative phase in the intima. Our findings strongly sugge
st that elastin synthesis and smooth muscle cell proliferation are tig
htly regulated during the repair of arterial wall injury.