TIPE2 deficiency accelerates neointima formation by downregulating smooth muscle cell differentiation

• DOI: 10.4161/cc.23325
• Publication Date: 2013-01-29T01:01:41Z
• Authors: Guizhong Zhang; Wenqian Zhang; Yunwei Lou; Wenjin Xi; Jian Cui; Minghong Geng; Faliang Zhu; Youhai H. Chen; Suxia Liu
• Keywords: Neointima; Calponin; Phenotypic switching

Phenotypic switching of vascular smooth muscle cells (VSMCs) is known to play a key role in the development atherosclerosis. However, mechanisms that mediate VSMC phenotypic are unclear. We report here TIPE2, tumor necrosis factor (TNF) α-induced protein 8-like 2 (TNFAIP8L2), plays an atheroprotective by regulating VSMCs response oxidized low-density lipoprotein (ox-LDL) stimuli. TIPE2-deficient treated with ox-LDL expressed lower levels contractile proteins such as SMαA, SM-MHC and calponin, whereas proliferation, migration synthetic capacity for growth factors cytokines were increased remarkably. Furthermore, TIPE2 inhibited proliferation preventing G 1/S phase transition. Interestingly, these effects on dependent P38 ERK1/2 kinase signals. As result, neointima formation was accelerated carotid arteries mice. These results indicate potential inhibitor