Continuous activation of angiotensin II (Ang II) induces renal vascular endothelial dysfunction, inflammation, and oxidative stress, all of which may contribute to renal damage. It is well established that microRNAs (miRNAs) play crucial regulatory roles in the pathogenesis of hypertensive renal damage. However, the detailed mechanisms and regulatory roles of miRNAs as therapeutic targets underlying Ang II-induced renal artery endothelial cell dysfunction in hypertensive renal damage have yet to be fully elucidated. The present study aimed to explore the expression status and putative role of miRNA-200c-3p in mediating the progression of hypertensive renal damage. We carried out real-time quantitative PCR (RT-qPCR) to detect the expression of miRNA-200c-3p in rat renal artery endothelial cells (RRAECs) induced by Ang II. MTT and transwell assays were utilized to evaluate the effects of miRNA-200c-3p on cell proliferation and migration, respectively. The present results revealed that the expression of miRNA-200c-3p was significantly upregulated in RRAECs exposed to Ang II compared with that of normal cells. miRNA-200c-3p overexpression markedly inhibited cell proliferation and migration of Ang II-induced RRAECs. Furthermore, bioinformatics predictions and dual-luciferase reporter assays indicated that zinc finger E-box-binding homeobox 2 (ZEB2) was a direct target gene of miRNA-200c-3p and that ZEB2 expression was inversely correlated with the levels of miRNA-200c-3p in RRAECs after exposure to Ang II. The effects of ZEB2 silencing were similar to the inhibitory effects observed following miRNA-200c-3p overexpression, and recovered ZEB2 expression reversed the anti-proliferative and anti-migratory influence of miRNA-200c-3p upregulation in RRAECs induced by Ang II. The present study indicated that miRNA-200c-3p might suppress the proliferation and migration of Ang II-induced RRAECs by targeting ZEB2. The miRNA-200c-3p/ZEB2 axis will provide valuable insights into the clinical management of hypertension-related kidney disease.

中文翻译：

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MicroRNA-200c-3p通过直接靶向ZEB2抑制肾动脉内皮细胞的增殖和迁移。

血管紧张素II（Ang II）的持续激活会诱发肾血管内皮功能障碍，炎症和氧化应激，所有这些都可能导致肾脏损害。众所周知，microRNA（miRNA）在高血压肾脏损害的发病机理中起着至关重要的调节作用。然而，miRNA作为高血压肾损伤中Ang II诱导的肾动脉内皮细胞功能障碍的治疗靶点的详细机制和调节作用尚未完全阐明。本研究旨在探讨miRNA-200c-3p在介导高血压肾损害进展中的表达状态和推定作用。我们进行了实时定量PCR（RT-qPCR），以检测miRNA-200c-3p在Ang II诱导的大鼠肾动脉内皮细胞（RRAEC）中的表达。使用MTT和transwell分析分别评估miRNA-200c-3p对细胞增殖和迁移的影响。目前的结果表明，与正常细胞相比，暴露于Ang II的RRAEC中miRNA-200c-3p的表达明显上调。miRNA-200c-3p的过表达显着抑制了Ang II诱导的RRAECs的细胞增殖和迁移。此外，生物信息学预测和双荧光素酶报告基因检测表明，锌指结合E-box的同源盒2（ZEB2）是miRNA-200c-3p的直接靶基因，而ZEB2表达与miRNA-200c-p的水平呈负相关。暴露于Ang II后的RRAEC中的3p。ZEB2沉默的作用类似于miRNA-200c-3p过表达后观察到的抑制作用，恢复的ZEB2表达逆转了Ang II诱导的RRAECs中miRNA-200c-3p上调的抗增殖和抗迁移的作用。本研究表明，miRNA-200c-3p可能通过靶向ZEB2抑制Ang II诱导的RRAEC的增殖和迁移。miRNA-200c-3p / ZEB2轴将为高血压相关肾脏疾病的临床管理提供有价值的见解。