MiR-217 inhibits apoptosis of atherosclerotic endothelial cells via the TLR4/PI3K/Akt/NF-κB pathway.

Objective To determine the effect of miR-217 on the apoptosis of atherosclerotic endothelial cells (AECs) through the Toll-like receptor (TLR) 4/PI3K/Akt/NF-κB pathway. Materials and methods Oxidized low-density lipoprotein (ox-LDL) was used to construct an atherosclerotic endothelial cell model, and the expression of miR-217/TLR4/PI3K/Akt/NF-κB in the cells was regulated to explore their effects on the viability, apoptosis, inflammatory factors [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10)], and endothelial-to-mesenchymal transformation (EndMT) of the endothelial cells. Results In AECs, miR-217 expression decreased, and the PI3K/Akt/NF-κB pathway was inhibited. The Dual-Luciferase reporter assay revealed that TLR4 was the target of miR-217, and it was up-regulated in AECs, and the further study revealed that up-regulation of miR-217 protected AECs, increased their activity, reduced their apoptosis, and inhibited inflammatory response and EndMT, while TLR4 acted contrary to miR-217. Besides, it was also found that miR-217 inhibited the PI3K/Akt/NF-κB pathway, thus weakening the influence of si-TLR4 on endothelial cells. Furthermore, miR-217 inhibited EndMT by inhibiting TLR4 from activating the PI3K/Akt/NF-κB signal pathway. Conclusions In AECs, TLR4 expression increased, and miR-217 and the PI3K/Akt/NF-κB signaling pathway are inhibited. Additionally, miR-217 can increase the viability of AECs through the TLR4/PI3K/Akt/ NF-κB signal transduction pathway, and inhibit their apoptosis, inflammatory response, and EndMT.