Intimal Thickening After Ligature of Arteries An Electron-Microscopic Study

Abstract

Concentric thickening of the tunica intima was observed in a short length of common carotid artery which had been tied off between two ligatures, and also in the pieces immediately proximal and distal to the doubly ligated part. The thickening was not due to hyperplasia of endothelial cells; in fact, the endothelium in the doubly ligated part was necrotic a short time after ligature. This piece then became lined with macrophage-like cells, thought to be derived from monocytes of the blood contained in the lumen. These cells retained quantities of colloidal thorium dioxide which had been given intravenously just be fore applying the ligatures. On the other hand, the thickening of the intima seen in the doubly ligated segment, as well as in the adjoining lengths of artery, was principally due to the growth of a cell derived from the smooth muscle of the tunica media, for which the term "myo-intimal" cell is suggested.

A monoclonal antibody (3G5)-defined ganglioside antigen is expressed on the cell surface of microvascular pericytes.

“…The relationship of pericytes to smooth muscle cells is also brought into question, as pericytes have been shown to express muscle type contractile proteins but the 3G5 antigen is not found on either smooth or skeletal muscle (10). Further studies pursuing our observation (unpublished) that aortic intimal cells, but not medial cells, express the 3G5 antigen may enable the question of the relationship of smooth muscle cells to pericytes to be addressed more fully, as the pericyte has been considered by some authors to be similar to the so called "myointimal cell" (27) and the intermediate cell of Robertson (28) and Page et al (29). These cells were considered to be dedifferentiated smooth muscle cells or to be derived by growth from smooth muscle cells of the tunica media (1).…”

Smooth Muscle Cells: To Be or Not To Be?

“…As cited in the commentary, one of the classical studies showed that, after artery ligation, the cells in the neointima had synthetic phenotype and differed from SMCs in ultrastructure, which was assumed to be dedifferentiated SMCs without rigorous cell tracing. 19 Similarly, the loss of the expression of SMC markers, such as SMA, SM-22α, and SM-MHC, in response to injury was attributed to the silence of these genes in SMCs in many previous studies. 20 It is intriguing that SMA and SM22α, the 2 immature SMC markers downregulated but not completely silenced in proliferative/synthetic SMCs, are not expressed in the vascular cells after the injury.…”

all- Trans -Retinoic Acid Reduces Neointimal Formation and Promotes Favorable Geometric Remodeling of the Rat Carotid Artery After Balloon Withdrawal Injury

“…1 Medial smooth muscle cell (SMC) dedifferentiation, growth, and migration are salient features of such intimal expansion. [2][3][4][5][6][7] Similar activities are thought to underlie the pathogenesis of atherosclerosis and a subset of human restenotic lesions. 8,9 Despite the intensive study of therapeutic agents aimed at arresting SMC growth and migration, no widely effective treatment exists for the prevention of human restenosis.…”