Duchenne muscular dystrophy (DMD) is the most frequent muscular dystrophy in children and young adults. Currently, there is no cure for the disease. The transplantation of healthy myoblasts is an experimental therapeutic strategy, since it could restore the expression of dystrophin in DMD muscles. Nevertheless, this cellular therapy is limited by immune reaction, low migration of the implanted cells, and high early cell death that could be at least partially due to anoikis. To avoid the lack of attachment of the cells to an extracellular matrix after the transplantation, which is the cause of anoikis, we tested the use of a fibrin gel for myoblast transplantation. In vitro, three concentrations of fibrinogen were compared (3, 20, and 50 mg/ ml) to form a fibrin gel. A stiffer fibrin gel leads to less degradability and less proliferation of the cells. A concentration of 3 mg/ml fibrin gel enhanced the differentiation of the myoblasts earlier as a culture in monolayer. Human myoblasts were also transplanted in muscles of Rag/mdx mice in a fibrin gel or in a saline solution (control). The use of 3 mg/ml fibrin gel for cell transplantation increased not only the survival of the cells as measured after 5 days but also the number of fibers expressing dystrophin after 21 days, compared to the control. Moreover, the fibrin gel was also compared to a prosurvival cocktail. The survival of the myoblasts at 5 days was increased in both conditions compared to the control but the efficacy of the prosurvival cocktail was not significantly higher than the fibrin gel.Key words: Duchenne muscular dystrophy (DMD); Fibrin gel; Cell transplantation; Cell survival; Graft success INTRODUCTIONproliferate and differentiate as myoblasts, which subsequently activate myogenic differentiation to fuse among themselves to form new myofibers (17,33). These Duchenne muscular dystrophy (DMD) is the most common genetic muscle disorder in children. The incimyoblasts can be proliferated in culture and transplanted in muscles to fuse together and form new fibers or to dence is about 1/3,500 live male births and currently there is no efficient treatment (15). The cause of DMD fuse with host myofibers, introducing in these hybrid fibers nuclei able to produce dystrophin in the case of is a severe deficiency of dystrophin, a major component of the dystrophin-glycoprotein complex in muscle fibers, DMD. Unfortunately, transplanted proliferating myogenic cells undergo rapid and massive cell death within responsible for the maintenance of sarcolemma integrity (10). Following the loss of a functional dystrophin proa few days following implantation into skeletal muscles, as a result of cell dissociation, trophic factor withdrawal, tein, the muscles of DMD patients progressively degenerate as a result of continuous myofiber necrosis, leading oxidative stress, excitotoxicity, hypoxia, and possibly anoikis. Anoikis is a type of apoptosis that is triggered to death into the second/third decade of the patient's life (17,31).by detachment from the extracellular ma...