BACKGROUND INFORMATION: DMD (Duchenne muscular dystrophy) is a devastating X-linked disorder characterized by progressive muscle degeneration and weakness. The use of cell therapy for the repair of defective muscle is being pursued as a possible treatment for DMD. Mesenchymal stem cells have the potential to differentiate and display a myogenic phenotype in vitro. Since liposuctioned human fat is available in large quantities, it may be an ideal source of stem cells for therapeutic applications. ASCs (adipose-derived stem cells) are able to restore dystrophin expression in the muscles of mdx (X-linked muscular dystrophy) mice. However, the outcome when these cells interact with human dystrophic muscle is still unknown. RESULTS: We show here that ASCs participate in myotube formation when cultured together with differentiating human DMD myoblasts, resulting in the restoration of dystrophin expression. Similarly, dystrophin was induced when ASCs were co-cultivated with DMD myotubes. Experiments with GFP (green fluorescent protein)-positive ASCs and DAPI (4',6-diamidino-2-phenylindole)-stained DMD myoblasts indicated that ASCs participate in human myogenesis through cellular fusion. CONCLUSIONS: These results show that ASCs have the potential to interact with dystrophic muscle cells, restoring dystrophin expression of DMD cells in vitro. The possibility of using adipose tissue as a source of stem cell therapies for muscular diseases is extremely exciting.
BACKGROUND INFORMATION: DMD (Duchenne muscular dystrophy) is a devastating X-linked disorder characterized by progressive muscle degeneration and weakness. The use of cell therapy for the repair of defective muscle is being pursued as a possible treatment for DMD. Mesenchymal stem cells have the potential to differentiate and display a myogenic phenotype in vitro. Since liposuctioned human fat is available in large quantities, it may be an ideal source of stem cells for therapeutic applications. ASCs (adipose-derived stem cells) are able to restore dystrophin expression in the muscles of mdx (X-linked muscular dystrophy) mice. However, the outcome when these cells interact with humandystrophic muscle is still unknown. RESULTS: We show here that ASCs participate in myotube formation when cultured together with differentiating humanDMD myoblasts, resulting in the restoration of dystrophin expression. Similarly, dystrophin was induced when ASCs were co-cultivated with DMD myotubes. Experiments with GFP (green fluorescent protein)-positive ASCs and DAPI (4',6-diamidino-2-phenylindole)-stained DMD myoblasts indicated that ASCs participate in human myogenesis through cellular fusion. CONCLUSIONS: These results show that ASCs have the potential to interact with dystrophic muscle cells, restoring dystrophin expression of DMD cells in vitro. The possibility of using adipose tissue as a source of stem cell therapies for muscular diseases is extremely exciting.
Authors: Carlos de Paula Eduardo; Patricia Moreira de Freitas; Marcella Esteves-Oliveira; Ana Cecília Corrêa Aranha; Karen Müller Ramalho; Alyne Simões; Marina Stella Bello-Silva; Jan Tunér Journal: Lasers Med Sci Date: 2010-07-17 Impact factor: 3.161
Authors: Naghmeh Naderi; Emman J Combellack; Michelle Griffin; Tina Sedaghati; Muhammad Javed; Michael W Findlay; Christopher G Wallace; Afshin Mosahebi; Peter Em Butler; Alexander M Seifalian; Iain S Whitaker Journal: Int Wound J Date: 2016-02-01 Impact factor: 3.315
Authors: Sébastien Goudenege; Didier F Pisani; Brigitte Wdziekonski; James P Di Santo; Claude Bagnis; Christian Dani; Claude A Dechesne Journal: Mol Ther Date: 2009-04-07 Impact factor: 11.454
Authors: Tatiana Jazedje; Paulo M Perin; Carlos E Czeresnia; Mariangela Maluf; Silvio Halpern; Mariane Secco; Daniela F Bueno; Natassia M Vieira; Eder Zucconi; Mayana Zatz Journal: J Transl Med Date: 2009-06-18 Impact factor: 5.531