Amniotic Fluid Stem Cells Restore the Muscle Cell Niche in a HSA‐Cre, SmnF7/F7 Mouse Model123. (24th July 2012)

• Record Type: Journal Article
• Authors: Piccoli, Martina; Franzin, Chiara; Bertin, Enrica; Urbani, Luca; Blaauw, Bert; Repele, Andrea; Taschin, Elisa; Cenedese, Angelo; Zanon, Giovanni Franco; André‐Schmutz, Isabelle; Rosato, Antonio; Melki, Judith; Cavazzana‐Calvo, Marina; Pozzobon, Michela; De Coppi, Paolo
• Is Part Of: Stem cells. Volume 30:Number 8(2012)
• Page Start: 1675
• Page End: 1684
• Publication Date: 2012-07-24
• Subjects: Amniotic fluid stem cells -- Muscle dystrophy -- Muscle stem cell niche -- Spinal muscular atrophy; Cloning -- Periodicals; Clone cells -- Periodicals; Stem cells -- Periodicals; Cell Differentiation -- Periodicals; Cell Division -- Periodicals; Clone Cells -- Periodicals; Hematopoietic Stem Cells -- Periodicals; Stem Cells -- Periodicals; 571.84
• DOI: 10.1002/stem.1134
• Languages: English
• ISSNs: 1066-5099

Abstract

Abstract: Mutations in the survival of motor neuron gene ( SMN1 ) are responsible for spinal muscular atrophy, a fatal neuromuscular disorder. Mice carrying a homozygous deletion of Smn exon 7 directed to skeletal muscle ( HSA‐Cre, Smn F7/F7 mice) present clinical features of human muscular dystrophies for which new therapeutic approaches are highly warranted. Herein we demonstrate that tail vein transplantation of mouse amniotic fluid stem (AFS) cells enhances the muscle strength and improves the survival rate of the affected animals. Second, after cardiotoxin injury of the Tibialis Anterior, only AFS‐transplanted mice efficiently regenerate. Most importantly, secondary transplants of satellite cells (SCs) derived from treated mice show that AFS cells integrate into the muscle stem cell compartment and have long‐term muscle regeneration capacity indistinguishable from that of wild‐type‐derived SC. This is the first study demonstrating the functional and stable integration of AFS cells into the skeletal muscle, highlighting their value as cell source for the treatment of muscular dystrophies. STEM Cells 2012;30:1675–1684