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Letter to the Editor |
Stefanie Dimmeler, Department of Internal Medicine III, J.W. Goethe University, Frankfurt, Germany
Department of Surgery, Ludwig-Maximilians-University, Munich, Germany
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
In response:
In the August 3, 2007 issue of Circulation Research, Ergün and Gehling suggested in a Letter to the Editor1 that the concept of nonbone marrow–derived endothelial progenitor cells as shown by our group in the March 2, 2007 issue of Circulation Research,2 could mostly be anticipated by previous publications including their own3–5 demonstrating the existence of vessel wall–derived endothelial progenitor cells. Of course, we truly appreciate and acknowledge the important work by these authors concerning the identification and characterization of vessel wall–derived endothelial progenitor cells,3–5 but would like to emphasize that these progenitor cells represent only one of the multiple possible sources for circulating endothelial lineage fated cells that contribute to postnatal neovascularization and have been described in our recent manuscript.2 Other sources such as vessel wall–derived mature endothelial cells and, most importantly, tissue-resident progenitor cells including liver and intestinal stem cells, which are not directly related to vessels and, thus, have not yet been committed to an endothelial fate, might also play a role. Specifically, in the parabiosis model as used in our studies, we detected homing and incorporation of circulating cells in the target limb muscles by means of expression of the reporter gene ß-galactosidase under the control of an endothelial tie2 promoter. This system was used to confirm the final endothelial fate of the circulating cells that had migrated into the ischemic muscles. Apparently, this model does not allow the conclusion that the cells must have had an endothelial (progenitor) cell origin before
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