Are restenosis cells containing nonmuscle myosin really vascular smooth muscle cells?

نویسنده

  • J T Beranek
چکیده

Are Restenosis Cells Containing Nonmuscle Myosin Really Vascular Smooth Muscle Cells? As a contributor to the study of restenosis,1-3 I have read with great attention the article by Leclerc et at4 and the Editorial Comment by Williams and Meidell5 about the evidence implicating nonmuscle myosin in restenosis. I would like to ask the authors4S why they use the term "smooth muscle cells" for the cells containing nonmuscle myosin. Unfortunately, Leclerc et a14 have not studied whether the cells containing nonmuscle myosin also possess smooth muscle myosin isoform. This question has been studied, however, by Zanellato et a6 in their outstanding experimental work concerning the myosin isoform expression in normal and atherosclerotic rabbit aortas. In the atherosclerotic plaque, which may be considered to be a model of the wound-healing reaction in the vascular wall, there are three populations of "vessel wall derived cells"7: 1) the cells containing only nonmuscle myosin, 2) the cells containing only smooth muscle myosin, and 3) the cells containing both isoforms.6 This suggests that the cells containing only nonmuscle myosin differentiate into smooth muscle cells but leaves open the question of their origin. At variance with Zanellato et al,6 I believe that the atherosclerotic cells containing only nonmuscle myosin originate in nonmuscle myosin-positive vascular endothelial cells. For example, the horizontal structure visualized at the bottom of their Figure liB is undoubtedly a hyperplastic capillary in the process of canalization and giving rise to interstitial fibroblastic cells.6'7 Indeed, from the "vessel wall derived cells,"7 only the undifferentiated vascular endothelial cells differentiating into smooth muscle cells are able to express macrophagic and smooth muscle cell markers concomitantly.8 At the same time, only this concept explains clearly why "blocking angiogenesis might block intimal hyperplasia, and vice versa."9

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عنوان ژورنال:
  • Circulation

دوره 86 1  شماره 

صفحات  -

تاریخ انتشار 1992