Electronic Letters to:
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Electronic letters published:
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Author's Response
- Wojtek Wojakowski, Magda Kucia, Maciej Kazmierski, Mariusz Z Ratajczak, and Michal Tendera (7 January 2008)
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Wojtek Wojakowski Silesian School of Medicine, Poland, Magda Kucia, Maciej Kazmierski, Mariusz Z Ratajczak, and Michal Tendera
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wojtek.wojakowski{at}gmail.com Wojtek Wojakowski, et al.
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Dear Editor, Thank you for forwarding us the leter of Dr Rochefort and his kind comments on the paper. He has made a good point, and of course he is right about the increased mobilization of the MSC in experimental hypoxia, which he confirmed in an elegant experiment. Table 3 contains an typing error, which we are sorry to have missed during proofreading. The correct meaning of the sentence is "Increase of bone marrow-dependent mesenchymal stem cells (rats)". Again I apologize for the mistake. Sincerely, Wojciech Wojakowski MD on behalf of the authors |
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Gael Y Rochefort, PhD INSERM U658, CHR ORLEANS, HOPITAL Porte Madeleine, BP 2439 45032, ORLEANS, CEDEX 1, France
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gael.rochefort{at}gmail.com Gael Y Rochefort
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Dear Editor, I read with great interest the review by Wojakowski et al about the mobilization of bone marrow-derived stem/progenitor cells during acute coronary syndromes.1 The contribution of such cells, including hematopoietic stem cells, mesenchymal stem cells (MSCs), endothelial progenitor cells and other poorly defined progenitors, is well in coronary heart diseases. I agree this review discusses and summarizes information regarding mechanisms of mobilization, homing and engraftment of stem/progenitor cells that may take part in cardiac repair after ischaemic injury. Among all factors that can modulate the number of circulating stem/progenitor cells, authors stated that “hypoxia induced a decrease of (circulating) bone marrow-derived MSCs” (table 3)1; however, the quoted references, authored by Rochefort et al, clearly demonstrated the opposite.2 In fact, Rochefort et al evidenced that firstly MSCs were regularly observed in the rat circulating blood and that secondly MSCs were consistently and dramatically mobilized into the bloodstream after chronic hypoxia.2 Although, mechanisms inducing such a mobilization during chronic hypoxia remain unclear, this hypoxia-induced mobilization model represents a great tool to study the in vivo effect of factors in the MSC mobilization process. To conclude, even if this specific point about the hypoxia-induced mobilization was incorrect, data reported in the review by Wojakowski et al were not affected and this excellent review is to be applauded. References 1. Wojakowski W, Kucia M, Kazmierski M, et al. 2. Rochefort G, Delorme B, Lopez A, et al. |
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