(Circulation. 2008;117:e307.)
© 2008 American Heart Association, Inc.
Correspondence |
Neufeld Cardiac Research Institute, Tel-Aviv University, Sheba Medical Center, Tel-Hashomer, Israel
The Advanced Technology Center, Sheba Medical Center, Tel-Hashomer, Israel
We appreciate the comments of Drs Sadek and Garry on our study.1 We agree that the competent immune system of the rat may have recognized the mesenchymal cells as foreign and eliminated those cells via cellular rejection. We also agree that studies with autologous stem cells or delivery of allogeneic stem cells into an immunocompromised host could improve the chance of cell survival and the probability of generating a true positive magnetic resonance imaging signal from the implanted cells. However, we disagree that the design of our study created misleading conclusions. Our study was not designed to confirm or refute the immunoprivileged properties of mesenchymal stem cells. We describe a scenario in which the magnetic resonance image continue to provide a positive signal from the superparamagnetic iron oxide marker despite the disappearance of the implanted, labeled cells. We showed that the reason for this finding emerged from the superparamagnetic iron oxide marker that was engulfed by resident macrophages. This may also occur after autologous stem cell transplantation, especially after long-time ex vivo expansion, as the cells may change their phenotype2 and may be rejected after transplantation. In addition, even autologous cells could die from other causes such as trauma, ischemia, or apoptosis. We believe that our model is suitable to demonstrate a clinically relevant scenario in which the implanted superparamagnetic iron oxide–labeled cells died and the magnetic resonance imaging signal arose from cardiac macrophages that engulfed the superparamagnetic iron oxide nanoparticles.1
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2. Zhang CC, Lodish HF. Murine hematopoietic stem cells change their surface phenotype during ex vivo expansion. Blood. 2005; 105: 4314–4320.
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