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DVT: A New Era in Anticoagulant Therapy Blockade of the Ras–Extracellular Signal–Regulated Kinase 1/2 Pathway Is Involved in Smooth Muscle 22–Mediated Suppression of Vascular Smooth Muscle Cell Proliferation and Neointima Hyperplasia Li-Hua Dong, Jin-Kun Wen, George Liu, Michael A. McNutt, Sui-Bing Miao, Rui Gao, Bin Zheng, Hailin Zhang, Mei Han 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 22 (SM22) on VSMC proliferation in vitro and in vivo and explored the potential molecular mechanisms of this effect. Methods and Results—By using coimmunoprecipitation and glutathione S-transferase pull-down assays, we have shown that SM22 binds to Ras in SM22-overexpressed VSMCs in the presence or absence of platelet-derived growth factor–BB stimulation. SM22 arrested cell cycle progression through segregation of Ras with Raf-1 and downregu- lation of the Raf-1–MEK1/2–extracellular signal–regulated kinase 1/2 mitogen-activated protein kinase signaling cascade. The inhibitory effect of SM22 on VSMC proliferation was verified in vivo. The infection of rat carotid arteries with recombinant adenovirus encoding SM22 inhibited neointimal hyperplasia via suppression of the Raf-1–MEK1/ 2–extracellular signal–regulated kinase 1/2 signaling pathway. Conclusion—These findings suggest
Arteriosclerosis, Thrombosis, and Vascular Biology – Wolters Kluwer Health
Published: Apr 1, 2010
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