The effects of selenium on the translation efficiency of selenoproteins Gpx1, Gpx4, and Txnrd1 in oxLDL-induced EA.hy926 cells

Selenium is a crucial trace element that contributes to physiological processes in the body as selenoproteins. Selenoproteins serve as an integral role in the body in controlling the redox state of cells and protecting against damage induced by oxidative stress. This study aimed to investigate the effects and possible mechanism of selenium on selenoproteins expression in EA.hy926 cells induced by oxLDL. The impact of selenium on the viability of EA.hy926 cells was detected by the MTT method, and intracellular ROS level and mitochondrial membrane potential were assessed by fluorescent probe DCFH-DA and JC-1, respectively. RNA-seq, quantitative real-time PCR (RT-qPCR), and western blot were used to investigate the selenoprotein expression. Selenoprotein mRNA translation efficiency was analyzed by ribosome profiling (Ribo-Seq) coupled with transcriptomics. Our data showed that selenium supplementation (0.5 μmol/L) significantly decreased ROS production, reduced mitochondrial inner membrane potential and increased the proliferative activity of EA.hy926 cells induced by oxLDL. Moreover, The protective effects of selenium against oxLDL-induced EA.hy926 cell injury were associated with the upregulation of the expressions of selenoproteins GPX1, GPX4, and TXNRD1. Furthermore, the expressions of selenoproteins GPX1 and GPX4 were hierarchically controlled, but the expressions of selenoproteins TXNRD1 were mainly regulated by oxLDL. Finally, Ribo-Seq coupled with transcriptomics results demonstrated that the expressions of selenoproteins GPX1, GPX4, and TXNRD1 were regulated at the translation process level. These findings suggested that selenium could have preventive effects in oxLDL induced EA.hy926 cell injury by regulating the selenoprotein expression, and the selenoproteins expressions at the translation level in vascular endothelial cells need further study.