| First Author | Zhang G | Year | 2013 |
| Journal | Cell Cycle | Volume | 12 |
| Issue | 3 | Pages | 501-10 |
| PubMed ID | 23324338 | Mgi Jnum | J:314786 |
| Mgi Id | MGI:6822528 | Doi | 10.4161/cc.23325 |
| Citation | Zhang G, et al. (2013) TIPE2 deficiency accelerates neointima formation by downregulating smooth muscle cell differentiation. Cell Cycle 12(3):501-10 |
| abstractText | Phenotypic switching of vascular smooth muscle cells (VSMCs) is known to play a key role in the development of atherosclerosis. However, the mechanisms that mediate VSMC phenotypic switching are unclear. We report here that TIPE2, the tumor necrosis factor (TNF) alpha-induced protein 8-like 2 (TNFAIP8L2), plays an atheroprotective role by regulating phenotypic switching of VSMCs in response to oxidized low-density lipoprotein (ox-LDL) stimuli. TIPE2-deficient VSMCs treated with ox-LDL expressed lower levels of contractile proteins such as SMalphaA, SM-MHC and calponin, whereas the proliferation, migration and the synthetic capacity for growth factors and cytokines were increased remarkably. Furthermore, TIPE2 inhibited VSMCs proliferation by preventing G 1/S phase transition. Interestingly, these effects of TIPE2 on VSMCs were dependent on P38 and ERK1/2 kinase signals. As a result, neointima formation was accelerated in the carotid arteries of TIPE2-deficient mice. These results indicate that TIPE2 is a potential inhibitor of atherosclerosis. |
