Inflammatory cytokines are important protagonists in the formation of atherosclerotic plaques, triggering effects throughout the atherosclerotic vessels due to the destruction in proliferation, migration and angiogenesis of endothelial cells. In this study, we found SNHG1 is upregulated in TNF-α-treated HUVECs. We silenced SNHG1 and found it inhibited vascular endothelial cell proliferation and angiogenesis. In the other hand, exogenetic overexpression of SNHG1 promotes proliferation, migration and angiogenesis. Then we demonstrated that SNHG1 may interact directly with miR-196a to act as a miR-196a sponge. Further, MAPK6 were predicted to be the target of miR-196a. So we blocked miR-196a, which increased expression level of MAPK6, enhanced cell proliferation, migration and angiogenesis. These data indicated that SNHG1/miR-196a/MAPK6 axis may take a part in autophagy regulation in TNF-α-treated HUVECs. The subsequent rescue experiments come to the results ascertained the specificity of SNHG1/miR-196a/MAPK6 axis in regulating MAPK6. Overall, our findings demonstrate a novel mechanism by which SNHG1 overexpression protects the function of HUVECs, which may delay the progression of AS. SNHG1/miR-196a/MAPK6 axis may be of therapeutic significance in AS.

中文翻译：

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LncRNA SNHG1通过miR-196a调节血管内皮细胞增殖和血管生成。

炎性细胞因子是动脉粥样硬化斑块形成中的重要角色，由于内皮细胞的增殖，迁移和血管生成受到破坏，因此在整个动脉粥样硬化血管中均具有触发作用。在这项研究中，我们发现SNHG1在TNF-α处理的HUVEC中被上调。我们沉默了SNHG1，发现它可以抑制血管内皮细胞增殖和血管生成。另一方面，SNHG1的外源性过表达促进增殖，迁移和血管生成。然后我们证明了SNHG1可能直接与miR-196a相互作用以充当miR-196a海绵。此外，MAPK6被预测为miR-196a的目标。因此，我们阻断了miR-196a，从而增加MAPK6的表达水平，增强细胞增殖，迁移和血管生成。这些数据表明，SNHG1 / miR-196a / MAPK6轴可能参与了TNF-α处理的HUVEC的自噬调节。随后的抢救实验得出了确定SNHG1 / miR-196a / MAPK6轴在调节MAPK6中的特异性的结果。总体而言，我们的发现表明SNHG1过表达保护HUVEC的功能的新机制，这可能会延迟AS的发展。SNHG1 / miR-196a / MAPK6轴可能在AS中具有治疗意义。