Key result
Medial smooth muscle cells drive early neointima formation following extensive endothelial injury.
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The present study was undertaken to determine the mechanism of neointima formation in rabbit arteries subjected to extensive endothelial desquamation. Endothelial cells were selectively removed from the abdominal aorta by passing an inflated balloon catheter through the vessel. The healing response was then studied serially for up to a week, when neointima formation had provided a virtually complete cover. In en face preparations, the early neointimal cells appeared in random locations; they did not develop in apposition to residual, healthy endothelium. The possibility of blood cell colonization was explored by inserting killed aortic homografts. Since these homografts showed neointima formation only close to the site of junction with the normal aorta and as a direct extension of healthy endothelium, the likelihood of significant blood cell colonization was deemed small. Histologic and electron microscopic sections provided evidence that the early neointimal cells in the healing aorta were derived from medial smooth muscle cells. Healing of the injured arterial intima was accompanied by thickening instead of prompt restoration to normal, and the thickened intima resembled an arteriosclerotic plaque. The present study thus supports the concept that arteriosclerosis is a disease involving proliferation of medial smooth muscle cells.
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Spaet et al. (1975) studied Arterial intimal injury. Endothelial desquamation via balloon catheter vs. Killed aortic homografts / normal aorta was evaluated on Mechanism and source of neointima formation. Following extensive endothelial desquamation in rabbit aortas, early neointimal cells were derived from medial smooth muscle cells rather than residual endothelium or blood cell colonization.
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