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Cellular accumulation in the intima of injured artery has generally been attributed to smooth muscle cell proliferation. Since smooth muscle cells in normal artery are found mainly in the media, migration of smooth muscle cells into the intima has been considered a necessary prerequisite for subsequent myointimal thickening. The nondividing medial cells would appear to have no role in the reparative process. We have investigated in the rat ballooned carotid the possibility that nondividing cells might also contribute to injury-induced intimal thickening. All proliferating smooth muscle cells were labeled by 3H-thymidine given by continuous intraperitoneal infusion. The amounts of 3H-thymidine used were not toxic and did not inhibit smooth muscle cell proliferation. Autoradiograms performed on histological cross-sections showed a progressive decrease in the fraction of unlabeled cells at 3, 7, and 14 days after carotid injury. However, the actual number of nondividing cells remained constant. The calculated growth fraction for the 14-day period was 40%. A substantial number of unlabeled cells was observed in the intima. These data have led us to conclude that only a small fraction of smooth muscle cells in an artery proliferate in response to the injury stimulus, and do so shortly after injury, or not at all. Furthermore, nondividing, as well as proliferating smooth muscle cells, can migrate and contribute, in a substantial way, to the increase in intimal smooth muscle cell number.
Clowes et al. (Tue,) studied this question.