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Loss of microRNA-132 predicts poor prognosis in patients with primary osteosarcoma |
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| Authors: | Jie Yang Tiantian Gao Jie Tang Haikang Cai Lijun Lin Shiping Fu |
| Affiliation: | 1. Orthopedics Department, 8th Hospital, Shanghai, 200235, China 2. Orthopedics Department, Xuhui Central Hospital, Shanghai, 200031, China 3. Orthopedics Department, Zhujiang Hospital The Southern Medical University, Guangzhou, 510282, China |
| Abstract: | ??2-glycoprotein I (??2-GPI) is a plasma glycoprotein with diverse functions, but the impact and molecular effects of ??2-GPI on vascular biology are as yet unclear. Based on the limited information available on the contribution of ??2-GPI to endothelial cells, we investigated the effect of ??2-GPI on cell growth and migration in human aortic endothelial cells (HAECs). The regulation of ??2-GPI as part of intracellular signaling in HAECs was also examined. Vascular endothelial growth factor (VEGF) is a pro-angiogenic factor that may regulate endothelial functions. We found that ??2-GPI dose-dependently inhibited VEGF-induced endothelial cell growth using the 3-(4,5-dimethylthiazol-2-yl)-2,5-dipenyl tetrazolium bromide assay and cell counts. Using wound healing and Boyden chamber assays, ??2-GPI remarkably reduced VEGF-increased cell migration at the physiological concentration. Furthermore, ??2-GPI suppressed VEGF-induced phosphorylation of VEGF receptor 2 (VEGFR2), extracellular signal-regulated kinase 1/2 (ERK1/2), and Akt. These results suggest that ??2-GPI plays an essential role in the down-regulation of VEGF-induced endothelial responses and may be a useful component for anti-angiogenic therapy. |
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