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microRNA-128: A New Tool in the Smooth Muscle Cell Plasticity Toolbox.

The vascular smooth muscle cell (VSMC) is responsible for maintaining vessel tone, supplying organs and tissues with oxygenand nutrient-rich blood according to their needs. In response to stress, VSMCs can reinvent themselves and transform from a contractile, fully differentiated state to a proliferative, mobile state, capable of synthesizing extracellular matrix and growth factors.1 To accomplish this transformation, VSMCs use transcriptional and posttranscriptional pathways to silence contractile and adhesion programs and activate synthetic and cell division programs, using a variety of VSMC-specific transcriptional and epigenetic tools. To maintain their contractile status, VSMCs express myocardin and SRF (serum response factor), which activate contractile genes MHY11 and ACTA.2 When synthetic and proliferative programs are triggered, KLF4 (Krüppel-like factor 4) and ELK1 (ETS transcription factor ELK1) are expressed and cause dissociation of the myocardin complex from gene promoters, enabling repression of the differentiation program. KLF4 can also recruit histone deacetylases and demethylases, altering chromatin accessibility of contractile genes.