Satellite cells were identified over 40 years ago through electron microscopy. At this point in time, it is widely believed that satellite cells are the commited stem cells of adult skeletal muscle. Their major function is to repair, revitalize, and mediate skeletal muscle tissue and growth by differentiating into myocytes. Satellite cells are normally non proliferative. They do become active, however, when skeletal muscle tissue is injured or heavily used during activities such as weight lifting or running. Satellite cells are located at the surface of the basal lamina of the myofiber. (7) (Take a look at a satellite cell) (Image from http://www.mdausa.org/publications/Quest/q75resup.html)

What is the significance of MyoD and Pax-7?

MyoD, a major MRF (see skeletal muscle) is only expressed when satellite cells are activated to proliferate and differentiate into primary myoblasts, which will then differentaite into cells of the myofibers. When MyoD is knocked out in mice, satellite cells express quicker differentiation into primary myoblasts. (7) This suggests that there may be an intermediate step in the differentiation of a satellite cell to a myogenic precursor cell. Another very important factor of satellite cells in that of Pax-7. Pax-7 is a homeobox gene. The exact role of Pax-7 in terms of satellite cells is unknown, however, one thing is clear: when without Pax-7, there are no satellite cells. In fact, mice lacking Pax-7 do not survive beyond 2 weeks. (Look at Pax-7 expression in a satellite cell) (7)

Do satellite cells possess plasticity?

It was originally thought that satellite cells were a commited, unilineal population of stem cells, meaning that they only have the potential to differentiate into cells of the skeletal muscle tissue. Now, however, experiments have been performed in mice to dispute this claim, and suggest that satellite cells possess plasticity:

How do BMP's show this?

Several experiments have been done with primary myoblasts (derived from stem cells). When these cells are treated with BMP's (bone morphogenetic proteins), they are able to differentiate into osteocytes. (Observe osteogenic expression due to treatment with BMP's) (8) When treated with adipogenic inducers such as fatty acids and thiazolidinediones, primary myoblasts have the potential to become adipocytes. (link to see image of treated skeletal muscle: "bmp") It was first thought that the primary myoblasts would de-differentiate into multi potential progenitor cells without specific lineage markers. However, with further research, it became known that when treated with BMP's, primary myoblasts expressed MyoD, Pax-7, desmin (see above and skeletal muscle), and ALP. ALP is an early osteogenic marker. Therefore, this suggests that primary myoblasts do not de-differentiate, but instead directly differentiate to osteocytes. (Look at ALP staining of muscle fibers) (8)

Is there any inherent plasticity?

Although primary myoblasts are not satellite cells (satellite cells are precursors to primary myoblasts), further experiments have shown that MyoD and Myf5 (see skeletal muscle) are virtually undectable in primary myoblasts on freshly isolated myofibers. Therefore, it is only natural to think that without MRF's such as these, satellite cells would possess increased plasticity. (8)

Finally, through even more studies, some scientists declare that there is a second population of satellite cells. These satellite cells are thought to be radiation resistant, because when injected into irradited mdx mice (which have muscular dystrophy), dystrophyn was formed (see bone marrow). (6)