Abstract
SM22α is a shape change and transformation sensitive 22 kDa actin-binding protein of the calponin family. It is ubiquitous to vascular and visceral smooth muscle, and is an early marker of smooth muscle differentiation. It is also present in fibroblasts, and some epithelium. SM22α may be involved in calcium-independent smooth muscle contraction. Recent evidence suggests that disruption of SM22α induces vascular inflammation and is involved in osteochondrogenesis in arterial diseases. This is consistent with activation of NF-κB signaling, where NF-κB activity is upregulated in vascular injury. High expression of SM22α inhibits cell proliferation in VSMCs and in injured arteries. SM22α acts as a tumor suppressor. Loss of its expression is an early event in cell transformation and the development of some tumors, coinciding with cellular plasticity.
Keywords: SM22α, Cellular plasticity, Vascular diseases
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