It was suggested that transient up-regulation of OPN after muscle injury plays a positive role in overall regeneration [26]; however, in cultured myoblasts OPN has been shown to inhibit cell migration and differentiation under some experimental conditions [27] and in pathologically inflamed muscle of MDX mice (animal model of DMD), OPN was shown to inhibit muscle regeneration [24]. This evidence concerns the gene SPP1 and Duchenne muscular dystrophy.