Phoenixin-14 has been reported to be implicated in the process of blood glucose metabolism, reproduction, lipid deposition and cardioprotection. However, the role of phoenixin-14 in vascular smooth muscle cells (VSMCs) remains unkown. In this study, we focused on the effects of phoenixin-14 on VSMCs under oxidized low-density lipoprotein (ox-LDL) treatment. The experimental results demonstrated that phoenixin-14 inhibited mRNA level and nuclear translocation of β-catenin. Functionally, phoenixin-14 inhibited cell proliferation and facilitated apoptosis of VSMCs under ox-LDL stimulation, and CTNNB1 overexpression reversed these effects. Mechanistically, KCNQ1OT1 interacted with miR-183-3p to upregulate CTNNB1 in VSMCs. Furthermore, CTNNB1 expression was negatively correlated with miR-183-3p but positively associated with KCNQ1OT1. Rescue assays indicated that KCNQ1OT1 overexpression or Lithium chloride (LiCl) treatment reversed the effects of phoenixin-14 on proliferation and apoptosis of ox-LDL-stimulated VSMCs. In summary, phoenixin-14 regulates proliferation and apoptosis of ox-LDL-treated VSMCs by regulating the KCNQ1OT1/miR-183-3p/CTNNB1 axis.

据报道，Phoenixin-14 与血糖代谢、繁殖、脂质沉积和心脏保护过程有关。然而，phoenixin-14 在血管平滑肌细胞 (VSMCs) 中的作用仍然未知。在本研究中，我们重点研究了氧化低密度脂蛋白 (ox-LDL) 处理下 phoenixin-14 对 VSMC 的影响。实验结果表明，phoenixin-14抑制了β-catenin的mRNA水平和核转位。在功能上，phoenixin-14 在 ox-LDL 刺激下抑制细胞增殖并促进 VSMC 的凋亡，而 CTNNB1 过表达逆转了这些作用。从机制上讲，KCNQ1OT1 与 miR-183-3p 相互作用以上调 VSMC 中的 CTNNB1。此外，CTNNB1 表达与 miR-183-3p 呈负相关，但与 KCNQ1OT1 呈正相关。救援试验表明，KCNQ1OT1 过表达或氯化锂 (LiCl) 处理逆转了 phoenixin-14 对 ox-LDL 刺激的 VSMC 增殖和凋亡的影响。总之，phoenixin-14 通过调节 KCNQ1OT1/miR-183-3p/CTNNB1 轴来调节 ox-LDL 处理的 VSMC 的增殖和凋亡。