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J Thorac Cardiovasc Surg 2001;121:820-821
© 2001 The American Association for Thoracic Surgery


Letters to the Editor

Reply

Makiko Ueda, MD

Department of Pathology, Osaka City University Medical School, Osaka, Japan

Reply to the Editor:

Beranek raises an interesting, albeit rather controversial point. Because of the presence of small turquoise dots in macrophages in our Fig 4, A and B, which show immunologic double staining for smooth muscle cells and macrophages, Beranek suggests that small fascicles of muscle fibrils are present within these macrophages. From this observation, and obviously being a proponent of the hypothesis that the vascular endothelial cell is the stem cell for neointimal formation after vessel wall injury, Beranek opines that the cells alluded to in Fig 4, A and B, stem from vascular endothelial cells. However, the mere presence of small turquoise dots does not justify such a far-reaching conclusion. The turquoise staining is much too diffuse, so that small dots occur not only within cells but also outside cells in the extracellular matrix, as one can see easily in the neointima in Fig 4, A. The idea of an endothelial stem cell origin of smooth muscle cells, moreover, is based mostly on in vitro studies of embryonic cells and, for the time being, remains largely hypothetical. Our study was not designed for this particular purpose and, therefore, does not provide scientific evidence to either support or deny the concept of transdifferentiation. However, our own previous studies,Go Go 1-3 as well as those of others,Go Go 4,5 have shown that proliferative activity resulting in neointimal formation follows a process of de-differentiation of smooth muscle cells, which makes it most unlikely that the response is due to proliferating endothelial stem cells.

12/8/113930doi:10.1067/mtc.2001.113930

References

  1. Ueda M, Becker AE, Tsukada T, Numano F, Fujimoto T. Fibrocellular tissue response after percutaneous transluminal coronary angioplasty: an immunocytochemical analysis of the cellular composition. Circulation 1991;83:1327-32.[Abstract/Free Full Text]
  2. Ueda M, Becker AE, Naruko T, Kojima A. Smooth muscle cell de-differentiation is a fundamental change preceding wound healing after percutaneous transluminal coronary angioplasty in humans. Coron Artery Dis 1995;6:71-81.[Medline]
  3. Takagi M, Ueda M, Becker AE, Takeuchi K, Takeda T. The Watanabe heritable hyperlipidemic rabbit is a suitable experimental model to study differences in tissue response between intimal and medial injury after balloon angioplasty. Arterioscler Thromb Vasc Biol 1997;17:3611-9.[Abstract/Free Full Text]
  4. Kocher O, Gabbiani F, Gabbiani G, Reidy MA, Cokay MS, Peters H, et al. Phenotypic features of smooth muscle cells during the evolution of experimental carotid artery intimal thickening. Lab Invest 1991;65:459-70.[Medline]
  5. Bai H, Matsuda J, Sawa Y, Nakano S, Shirakura R, Shimazaki Y, et al. Neointima formation after vascular stent implantation: spatial and chronological distribution of smooth muscle cell proliferation and phenotypic modulation. Arterioscler Thromb 1994;14:1846-53.[Abstract/Free Full Text]




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