| First Author | Tang Y | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 475 |
| Issue | 2 | Pages | 182-8 |
| PubMed ID | 27181356 | Mgi Jnum | J:235760 |
| Mgi Id | MGI:5800632 | Doi | 10.1016/j.bbrc.2016.05.068 |
| Citation | Tang Y, et al. (2016) ox-LDL induces endothelial dysfunction by promoting Arp2/3 complex expression. Biochem Biophys Res Commun 475(2):182-8 |
| abstractText | Oxidized low-density lipoproteins (ox-LDL) play a critical role in endothelial injury including cytoskeleton reorganization, which is closely related to actin-related protein 2/3 (Arp2/3) complex. The aim of this study was to investigate the role of Arp2/3 complex in ox-LDL-induced endothelial dysfunction. In this study, we found that Arp2 and Arp3 expression was increased under atherosclerotic conditions both in ApoE-/- mice and in ox-LDL-stimulated human coronary artery endothelial cells (HCAECs). Arp2/3 complex inhibitor CK666 significantly reduced ox-LDL-induced ROS generation and cytoskeleton reorganization, and increased NO release in HCAECs. Pretreatment with LOX-1- but not CD36-blocking antibody markedly decreased ox-LDL-induced Arp2 and Arp3 expression. Moreover, Rac-1 siRNA remarkably suppressed ox-LDL-stimulated Arp2 and Arp3 expression. Additionally, CK666 reduced endothelial nitric oxide synthase (eNOS) expression and atherosclerotic lesions in ApoE-/- mice. Collectively, ox-LDL induces endothelial dysfunction by activating LOX-1/Rac-1 signaling and upregulating Arp2/3 complex expression. |
