Atorvastatin Inhibits Balloon Injury-Induced Myocardin Expression and Carotid Intimal Hyperplasia in Adult Rat

Background and purpose: The use of statin has been documented to be effective to inhibit vascular smooth muscle cell (VSMC) hypertrophy. Myocardin, a cardiac regulated gene, is up-regulated in VSMC hypertrophy. However, the effect of statin on myocardin expression due to balloon injury-induced carotid intimal hyperplasia is little known. Methods: To evaluate the effect of statin on myocardin expression and VSMC hypertrophy, balloon injury to carotid artery of adult Sprague-Dawley rats was performed to induce VSMC hypertrophy. Atorvastatin (30 mg/kg) was given per day after surgery for 14 days. Results: Both myocardin mRNA and protein increased significantly after balloon injury to carotid artery, which was inhibited by either myocardin small interfering RNA (siRNA) or atorvastatin. Increased intimal areas and decreased lumen to intima ratios of carotid artery were noted after balloon injury, which was also inhibited by myocardin siRNA and atorvastation. Increased immunohistochemical labelings of myocardin and smooth muscle (SM) actin in the VSMCs of carotid artery were observed and atorvastatin or myocardin siRNA again reversed the labelings. Conclusions: Both myocardin protein and myocardin mRNA expressions were up-regulated in the rat model of balloon injury-induced VSMC hypertrophy. Treatment with atorvastatin or myocardin siRNA is associated with a reversal of abnormal regulation of myocardin in the hypertrophic VSMC of carotid artery.