The proliferation and migration of vascular smooth muscle cells (VSMCs) are one of the key regulatory links of atherosclerosis (AS). Long noncoding RNAs (lncRNAs) are emerging as key regulators in AS development. In this study, we first assessed the expression level of smooth muscle and endothelial cell‐enriched migration/differentiation‐associated lncRNA (SENCR) in the plasma of patients with coronary heart disease (CHD) and its predictive and diagnostic value. Second, we investigated the role of SENCR in the regulation network of human aortic‐VSMCs (HA‐VSMCs) proliferation and migration and determined its downstream regulatory mechanism. The results showed that SENCR was downregulated in the peripheral blood of CHD, and negatively related to the Gensini score. SENCR was enriched in HA‐VSMCs and mainly distributed in cytoplasm. Overexpression of SENCR significantly inhibited HA‐VSMCs proliferation, migration, and block cell cycle, while the knockdown of SENCR had the opposite effects. Moreover, bioinformatics analysis and luciferase reporter assay demonstrated that miR‐4731‐5p could directly bind to SENCR. Besides, we proved that FOXO3a inhibited HA‐VSMCs proliferation and migration by binding to the 3′‐untranslated region of miR‐4731‐5p. In summary, our research suggested that SENCR affects HA‐VSMCs proliferation and migration via regulating the miR‐4731‐5p/FOXO3a pathway.

中文翻译：

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长期非编码RNA SENCR调节血管平滑肌细胞增殖和迁移机制的初步研究。

血管平滑肌细胞（VSMC）的增殖和迁移是动脉粥样硬化（AS）的关键调控环节之一。长的非编码RNA（lncRNA）逐渐成为AS开发中的关键调控因子。在这项研究中，我们首先评估了冠心病（CHD）患者血浆中平滑肌和内皮细胞富集的迁移/分化相关lncRNA（SENCR）的表达水平及其预测和诊断价值。其次，我们研究了SENCR在人类主动脉-VSMC（HA-VSMC）增殖和迁移的调控网络中的作用，并确定了其下游调控机制。结果表明，SENCR在冠心病的外周血中被下调，与Gensini评分呈负相关。SENCR富含HA-VSMC，主要分布在细胞质中。SENCR的过表达显着抑制了HA-VSMC的增殖，迁移和阻断细胞周期，而SENCR的抑制作用则相反。此外，生物信息学分析和荧光素酶报告基因检测结果表明，miR-4731-5p可直接与SENCR结合。此外，我们证明FOXO3a通过与miR-4731-5p的3'-非翻译区结合来抑制HA-VSMC的增殖和迁移。总而言之，我们的研究表明，SENCR通过调节miR-4731-5p / FOXO3a途径影响HA-VSMC的增殖和迁移。我们证明FOXO3a通过与miR-4731-5p的3'-非翻译区结合来抑制HA-VSMC的增殖和迁移。总而言之，我们的研究表明，SENCR通过调节miR-4731-5p / FOXO3a途径影响HA-VSMC的增殖和迁移。我们证明FOXO3a通过与miR-4731-5p的3'-非翻译区结合来抑制HA-VSMC的增殖和迁移。总而言之，我们的研究表明SENCR通过调节miR-4731-5p / FOXO3a途径影响HA-VSMC的增殖和迁移。