Smooth muscle 22 alpha maintains the differentiated phenotype of vascular smooth muscle cells by inducing filamentous actin bundling

Abstract

Aim Smooth muscle 22 alpha (SM22α) is not required for the development and basal homeostatic function of smooth muscle cells (SMCs). However, a recent study demonstrated that SM22α plays a role in inhibiting the phenotypic modulation of vascular SMCs (VSMCs) from contractile to synthetic/proliferative cells. The present study investigated the mechanism underlying the SM22α-mediated maintenance of the contractile phenotype of VSMCs. Main methods The redifferentiation of synthetic SMCs was induced by serum deprivation for 48–72 h. The expression plasmids containing full-length cDNA of rat SM22α and a vector expressing SM22α antisense transcripts were constructed, respectively. Coimmunoprecipitation, cosedimentation assay and immunofluorescence analyses were used to detect the interaction of SM22α with F-actin. Key findings The results revealed that SM22α directly interacted and colocalized with F-actin and thus participated in the organization of the actin cytoskeleton in differentiated VSMCs. SM22α facilitated the assembly of actin filaments into bundles. The blockade of SM22α expression by SM22α antisense RNA led to the thinning and dispersion of actin filaments. Consequently, the ratio of F-actin to globular (G)-actin was reduced, and the cell contractility was lost. Significance The SM22α-induced F-actin bundling enhances the contractility and mobility of VSMCs, and the activity of SM22α is necessary for maintaining the differentiated phenotype of VSMCs.