Msx1 is correlated with muscle cell dedifferentiation. However, msx1 is also highly expressed in chondrocytes and is induced by BMP/TGF? signaling. Thus, although we observed a significant induction of msx1 expression upon chondrogenic differentiation in the satellite cells, it does not indicate whether the satellite cells have undergone dedifferentiation. Regardless, our data support that muscle progenitor cells that normally would undergo myogenesis, can be redirected to adopt a cartilage cell fate in vitro and in vivo. In this study, we have evaluated cartilage gene expression in the muscle progenitor cells that contribute to fracture healing. However, other cell types located in the vicinity of bone may also participate in cartilage and bone formation. Elegant grafting experiments using LacZ-positive donor mice and Lac-Z-negative recipients revealed that cells from the perichondrium, the fibrous covering of the bone, differentiate into chondrocytes and osteocytes during fracture Catharanthine sulfate repair. Cells associated with blood vessels, such as pericytes, have also been shown to have the ability to differentiate into chondrocytes. Cells that are positive for Tie-2, an endothelial cell marker, while not yet shown to be recruited to the fracture callus, are known to contribute to cartilage and bone formation during heterotopic ossification. Because of the diverse cell types that participate in cartilage formation during fracture healing, it is likely that these different types of cells use different signaling mechanisms when undergoing chondrogenic differentiation. It is known that TGF?, BMP, PTH, as well as Wnt signaling are all activated during fracture healing, and downstream molecules such as Smad, prostaglandin, Cox-2 and ?-catenin regulate this process. Our work demonstrates that transcription factors Pax3, Nkx3.2 and Sox9 regulate chondrogenic differentiation of muscle progenitor cells. However, it is unclear whether Nkx3.2 and Sox9 also participate in the chondrogenic differentiation of other cell types, such as perichondrial or endothelial cells, and how these different cell types coordinate their signaling events during fracture healing. The understanding of such signaling processes in different cell types may help to accelerate fracture healing. Pax3, Nkx3.2 and Sox9 are all known to play important roles during development. In embryogenesis, Pax3 is expressed in the dermomyotome of the somite, which gives rise to muscle cell precursors. Pax3 mutant mice exhibit somite truncations with loss of hypaxial dermomyotome, and absence of limb muscle. Our data support the role of Pax3 in promoting 
myogenesis in muscle satellite cells. Furthermore, our data shows that Pax3 has an additional function of inhibiting chondrogenic differentiation of muscle satellite cells. It was reported that constitutive expression of Pax3 led to increased proliferation and decreased cell size in satellite cells. We found that Pax3-infected cells had a much more elongated appearance as compared to the control cells cultured in the chondrogenic medium, although we could not clearly distinguish the differences in cell shape due to cell condensation that accompanies chondrogenesis. In the double knockout of Pax3 and its paralogue Pax7, significant cell death takes place, leading to the loss of most muscle fibers. In addition, Pax3 and Pax7 double mutant cells were found in the forming rib, Pimozide suggesting that they may have adopted a cartilage fate.