17β-estradiol upregulates striatin protein levels via Akt pathway in human umbilical vein endothelial cells.

17β-estradiol (E2) has been shown to have beneficial effects on the cardiovascular system. We previously demonstrated that E2 increases striatin levels and inhibits migration in vascular smooth muscle cells. The objective of the present study was to investigate the effects of E2 on the regulation of striatin expression in human umbilical vein endothelial cells (HUVECs). We demonstrated that E2 increased striatin protein expression in a dose- and time-dependent manner in HUVECs. Pretreatment with ICI 182780 or the phosphatidylinositol-3 kinase inhibitor, wortmannin, abolished E2-mediated upregulation of striatin protein expression. Treatment with E2 resulted in Akt phosphorylation in a time-dependent manner. Moreover, silencing striatin significantly inhibited HUVEC migration, while striatin overexpression significantly promoted HUVEC migration. Finally, E2 enhanced HUVEC migration, which was inhibited by silencing striatin. In conclusion, our results demonstrated that E2-mediated upregulation of striatin promotes cell migration in HUVECs.

17β - 雌二醇（E2）已被证明对心血管系统具有有益作用。我们先前证明E2可增加血管平滑肌细胞中纹蛋白水平并抑制其迁移。本研究的目的是探讨E2对人脐静脉内皮细胞（HUVECs）中纹蛋白表达的调节作用。我们证明E2在HUVECs中以剂量和时间依赖的方式增加纹蛋白的表达。用ICI 182780或磷脂酰肌醇 - 3激酶抑制剂渥曼青霉素预处理，可消除E2介导的纹蛋白表达上调。E2处理以时间依赖的方式导致Akt磷酸化。此外，沉默纹蛋白显著抑制HUVEC迁移，而纹蛋白过表达则显著促进HUVEC迁移。最后，E2增强HUVEC迁移，而沉默纹蛋白可抑制这种迁移。总之，我们的结果表明，E2介导的纹蛋白上调促进了HUVECs中的细胞迁移。