Yanxu Song, Xingguang Zhu, Xiangang Cai, Yinling Yu, Di Hu
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引用次数: 0
摘要
背景：研究了长非编码RNA（MBNL1-AS1）在诊断高血压患者动脉粥样硬化（AS）风险中的临床作用，以及MBNL1-AS1在血管紧张素II（Ang II）诱导下对血管平滑肌细胞（VSMC）的影响：方法：招募高血压患者评估 MBNL1-AS1 的表达。对 MBNL1-AS1 的显著性进行了 ROC 曲线和 Spearman 分析。用 Ang II（10-5 mol/L）处理人 VSMC，建立高血压细胞模型。MTT 和 Transwell 室用于细胞模型的增殖和迁移检测。通过荧光素酶活性验证了 MBNL1-AS1 的靶标。通过 GO 和 KEGG 分析研究了 miR-424-5p 共享靶点的功能富集：结果：在颈动脉内膜中层厚度（cIMT）增加的患者中观察到 MBNL1-AS1 的增加。MBNL1-AS1可预测强直性脊柱炎的风险，并与cIMT水平相关。敲除 MBNL1-AS1 可通过抑制 miR-424-5p 减轻 Ang II 对细胞增殖和迁移的影响。富集分析证实，miR-424-5p的靶点主要涉及丝氨酸/苏氨酸激酶活性、MAPK信号通路和PI3K-Akt信号通路：结论：MBNL1-AS1/miR-424-5p轴与高血压诱导的强直性脊柱炎的进展有关。
LncRNA MBNL1-AS1 functions as an alternative atherosclerosis biomarker in elderly hypertensive patients and regulates vascular smooth muscle cell function.
Background: The clinical role of long non-coding RNA (MBNL1-AS1) in diagnosing atherosclerosis (AS) risks of hypertensive patients and the effects of MBNL1-AS1 on vascular smooth muscle cells (VSMCs) triggered by angiotensin II (Ang II) were investigated.
Methods: The hypertensive patients were recruited to assess MBNL1-AS1 expression. The ROC curve and Spearman analysis was performed for the significance of MBNL1-AS1. Human VSMCs were treated with Ang II (10-5 mol/L) to establish a hypertensive cell model. MTT and Transwell chamber were used in proliferative and migratory detection of cell models. Targets of MBNL1-AS1 were verified by luciferase activity. Functional enrichment of shared targets of miR-424-5p was researched by GO and KEGG analysis.
Results: An increase of MBNL1-AS1 was observed in patients with increased carotid intima-media thickness (cIMT). MBNL1-AS1 could predict the risk of AS and related to cIMT levels. The knockdown of MBNL1-AS1 mitigated the influence of Ang II on cellular proliferation and migration by inhibiting miR-424-5p. Enrichment analysis corroborated that targets of miR-424-5p were mainly involved in serine/threonine kinase activity, MAPK signaling pathway, and PI3K-Akt signaling pathway.
Conclusions: MBNL1-AS1/miR-424-5p axis was connected with the progression of AS induced by hypertension.
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