Myocardin was shown to be a specific transcription factor that plays a central role in smooth muscle differentiation….Using several assays, we could show that the myocardin is lost at the point where slow growing cells are converted into fast growers we also found that myocardin expression is essential for their differentiation (Milyavsky et al., 2007). The unique contractile properties of the SMC lineage are directed by SRF/myocardin-regulated genes encoding SMC-restricted contractile proteins…. In the next picture we can see how this differentiation happends:

The fibroblast (immature cell)when exposed to a Growth factor (TGF-β1) increases assembly of a muscle filament called F-actin, inducing the myocardin-related transcription factor (MRTF)-A/B to go into the nucleus. After enter the nucleos, MRTF binds to serum response factor (SRF), and promote expression of a contractile gene program…. Program? yes, a group of other proteins tha regulate gene cell muscle differentiation. This group is called CArG-containing genes  and the members are α-actin (SMαA), SMγA, SM22-α, h1-calponin, and vinculin. The expression of these genes causes changes to the cytoskeleton, resulting in differentiation of the myofibroblast and the development of contractile function…. so this is another way to keep studying how smooth muscle proliferates in lung vessels… is essencial to understand how this happens to keep looking  for a therapy to hypertension.