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Journal of Translational Medicine

, 7:6

First Online: 14 January 2009Received: 21 October 2008Accepted: 14 January 2009DOI: 10.1186-1479-5876-7-6

Cite this article as: Jazedje, T., Secco, M., Vieira, N.M. et al. J Transl Med 2009 7: 6. doi:10.1186-1479-5876-7-6


The dystrophin gene, located at Xp21, codifies dystrophin, which is part of a protein complex responsible for the membrane stability of muscle cells. Its absence on muscle causes Duchenne Muscular Dystrophy DMD, a severe disorder, while a defect of muscle dystrophin causes Becker Muscular Dystrophy DMB, a milder disease. The replacement of the defective muscle through stem cells transplantation is a possible future treatment for these patients. Our objective was to analyze the potential of CD34+ stem cells from umbilical cord blood to differentiate in muscle cells and express dystrophin, in vitro. Protein expression was analyzed by Immunofluorescence, Western Blotting WB and Reverse Transcriptase – Polymerase Chain Reaction RT-PCR. CD34+ stem cells and myoblasts from a DMD affected patient started to fuse with muscle cells immediately after co-cultures establishment. Differentiation in mature myotubes was observed after 15 days and dystrophin-positive regions were detected through Immunofluorescence analysis. However, WB or RT-PCR analysis did not detect the presence of normal dystrophin in co-cultures of CD34+ and DMD or DMB affected patients- muscle cells. In contrast, some CD34+ stem cells differentiated in dystrophin producers- muscle cells, what was observed by WB, reinforcing that this progenitor cell has the potential to originate muscle dystrophin in vitro, and not just in vivo like reported before.

Electronic supplementary materialThe online version of this article doi:10.1186-1479-5876-7-6 contains supplementary material, which is available to authorized users.

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Autor: Tatiana Jazedje - Mariane Secco - Natássia M Vieira - Eder Zucconi - Thomaz R Gollop - Mariz Vainzof - Mayana Zatz


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