Adult muscle satellite cells are muscle stem cells that are responsible for adult myogenesis. Previous studies by our group showed that inhibition of phosphatidylinosito 3-kinase (PI3K) in C2C12 cells can inhibit myogenic differentiation. However, it remains unknown whether the PI3K signaling pathway can function in primary myoblasts and in vivo. In this study, an inhibitor of PI3K was used in primary myoblasts and single myofibers. We demonstrated that the PI3K signaling is required for muscle differentiation and that inhibition of the PI3K signaling cause a reduced proliferation and activation rate.

In addition, it was reported that both skeletal muscle and brown adipose tissue arise from Pax7 and Myf5 positive progenitors. In addition, overexpression of Prdm16 can convert myoblas...[ Read more ]

Adult muscle satellite cells are muscle stem cells that are responsible for adult myogenesis. Previous studies by our group showed that inhibition of phosphatidylinosito 3-kinase (PI3K) in C2C12 cells can inhibit myogenic differentiation. However, it remains unknown whether the PI3K signaling pathway can function in primary myoblasts and in vivo. In this study, an inhibitor of PI3K was used in primary myoblasts and single myofibers. We demonstrated that the PI3K signaling is required for muscle differentiation and that inhibition of the PI3K signaling cause a reduced proliferation and activation rate.

In addition, it was reported that both skeletal muscle and brown adipose tissue arise from Pax7 and Myf5 positive progenitors. In addition, overexpression of Prdm16 can convert myoblasts into adipocytes, while knockdown of Prdm16 in brown preadipocytes can turn them into muscle cells. Therefore, myoblasts and adipocytes have the potential to transdifferentiate into each other under defined conditions. However, the mechanisms that suppress the alternative cell fate in either myoblasts or brown adipocytes are still unknown. In this study, we demonstrated that knockdown of Pax7, MyoD or Myf5 in primary myoblasts or C2C12 cells can turn them into brown adipocytes. In addition, up-regulation of Prdm16 and C/EBPα were observed after knocking down MyoD and Myf5 in myoblasts. Therefore, we identified a pathway consisting of Pax7/MyoD/Myf5/PRDM16 in myoblasts that functions to suppress the fate of brown adipocytes.