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Objective— Vascular smooth muscle cells (VSMCs) can switch between differentiated and dedifferentiated phenotypes, and this phenotype switch is believed to be essential for repair of vascular injury. We studied the inhibitory effect of smooth muscle 22α (SM22α) on VSMC proliferation in vitro and in vivo and explored the potential molecular mechanisms of this effect.Methods and Results— By using coimmunoprecipitation and glutathioneS -transferase pull-down assays, we have shown that SM22α binds to Ras in SM22α-overexpressed VSMCs in the presence or absence of platelet-derived growth factor–BB stimulation. SM22α arrested cell cycle progression through segregation of Ras with Raf-1 and downregulation of the Raf-1–MEK1/2–extracellular signal–regulated kinase 1/2 mitogen-activated protein kinase signaling cascade. The inhibitory effect of SM22α on VSMC proliferation was verified in vivo. The infection of rat carotid arteries with recombinant adenovirus encoding SM22α inhibited neointimal hyperplasia via suppression of the Raf-1–MEK1/2–extracellular signal–regulated kinase 1/2 signaling pathway.Conclusion— These findings suggest that high expression of SM22α inhibits cell proliferation via reduction of the response to mitogen stimuli in VSMCs and provide a novel mechanism by which VSMCs maintain their contractile phenotype and resist mitogenic stimuli in an SM22α-dependent manner.

arteriosclerosis, thrombosis, and vascular biology

Blockade of the Ras–Extracellular Signal–Regulated Kinase 1/2 Pathway Is Involved in Smooth Muscle 22α–Mediated Suppression of Vascular Smooth Muscle Cell Proliferation and Neointima Hyperplasia