Mir-217 Inhibits Apoptosis Of Atherosclerotic Endothelial Cells Via The Tlr4/Pi3k/Akt/Nf-Kappa B Pathway
EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES(2020)
摘要
OBJECTIVE: To determine the effect of miR-217 on the apoptosis of atherosclerotic endothelial cells (AECs) through the Tolllike receptor (TLR) 4/PI3K/Akt/NF-kappa B 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-kappa B in the cells was regulated to explore their effects on the viability, apoptosis, inflammatory factors [tumor necrosis factor-alpha (TNF-alpha), 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-kappa B 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-kappa B pathway, thus weakening the influence of si-TLR4 on endothelial cells. Furthermore, miR-217 inhibited EndMT by inhibiting TLR4 from activating the PI3K/Ak/NF-kappa B signal pathway.CONCLUSIONS: In AECs. TLR4 expression increased, and miR-217 and the PI3K/Akt/NF-kappa B signaling pathway are inhibited. Additionally, miR-217 can increase the viability of AECs through the TLR4/PI3K/Akt/NF-kappa B signal transduction pathway, and inhibit their apoptosis. inflammatory response, and EndMT.
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关键词
MiR-217, Toll-like receptor 4, PI3K/Akt/NF-kappa B pathway, Endothelial cell
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