| First Author | Zhou Y | Year | 2016 |
| Journal | PLoS One | Volume | 11 |
| Issue | 5 | Pages | e0154720 |
| PubMed ID | 27144886 | Mgi Jnum | J:248832 |
| Mgi Id | MGI:6094401 | Doi | 10.1371/journal.pone.0154720 |
| Citation | Zhou Y, et al. (2016) PPARgamma Inhibits VSMC Proliferation and Migration via Attenuating Oxidative Stress through Upregulating UCP2. PLoS One 11(5):e0154720 |
| abstractText | Increasing evidence showed that abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) are common event in the pathophysiology of many vascular diseases, including atherosclerosis and restenosis after angioplasty. Among the underlying mechanisms, oxidative stress is one of the principal contributors to the proliferation and migration of VSMCs. Oxidative stress occurs as a result of persistent production of reactive oxygen species (ROS). Recently, the protective effects of peroxisome proliferator-activated receptor gamma (PPARgamma) against oxidative stress/ROS in other cell types provide new insights to inhibit the suggests that PPARgamma may regulate VSMCs function. However, it remains unclear whether activation of PPARgamma can attenuate oxidative stress and further inhibit VSMC proliferation and migration. In this study, we therefore investigated the effect of PPARgamma on inhibiting VSMC oxidative stress and the capability of proliferation and migration, and the potential role of mitochondrial uncoupling protein 2 (UCP2) in oxidative stress. It was found that platelet derived growth factor-BB (PDGF-BB) induced VSMC proliferation and migration as well as ROS production; PPARgamma inhibited PDGF-BB-induced VSMC proliferation, migration and oxidative stress; PPARgamma activation upregulated UCP2 expression in VSMCs; PPARgamma inhibited PDGF-BB-induced ROS in VSMCs by upregulating UCP2 expression; PPARgamma ameliorated injury-induced oxidative stress and intimal hyperplasia (IH) in UCP2-dependent manner. In conclusion, our study provides evidence that activation of PPARgamma can attenuate ROS and VSMC proliferation and migration by upregulating UCP2 expression, and thus inhibit IH following carotid injury. These findings suggest PPARgamma may represent a prospective target for the prevention and treatment of IH-associated vascular diseases. |
