Dysregulation of the proliferation and migration of vascular smooth muscle cells (VSMCs) is a crucial cause of atherosclerosis. MiR-637 exerts an antiproliferative effect on multiple human cells. Its impact on atherosclerosis remains largely unexplored. Real-time PCR was used to determine miR-637 expression in samples from atherosclerosis patients and animal models. Its expression in VSMC dysfunction models (induced by ox-LDL) was also measured. The proliferation and migration of VSMCs were respectively tested using CCK-8 and Transwell assays, and apoptosis was measured using flow cytometry. The Targetscan database was used to predict the target genes of miR-637. Interaction between miR-637 and the potential target gene was validated via real-time PCR, western blotting and a luciferase reporter assay. MiR-637 expression was significantly lower in atherosclerosis patient and animal model samples. It also decreased in a dose- and time-dependent manner in animal models with ox-LDL-induced atherosclerosis. Transfection with miR-637 mimics suppressed the proliferation and migration of VSMCs while promoting apoptosis, while transfection with miR-637 inhibitors had the opposite effects. We also validated that insulin-like growth factor-2 (IGF-2), a crucial factor in the pathogenesis of atherosclerosis, serves as a target gene for miR-637. MiR-637 targeting IGF-2 contributes to atherosclerosis inhibition and could be a potential target for this disease.

中文翻译：

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miR-637 的下调通过调节胰岛素样生长因子-2 促进血管平滑肌细胞增殖和迁移。

血管平滑肌细胞（VSMCs）的增殖和迁移失调是动脉粥样硬化的重要原因。MiR-637 对多种人体细胞具有抗增殖作用。它对动脉粥样硬化的影响在很大程度上仍未得到探索。实时荧光定量 PCR 用于确定来自动脉粥样硬化患者和动物模型的样品中 miR-637 的表达。还测量了其在 VSMC 功能障碍模型（由 ox-LDL 诱导）中的表达。分别用CCK-8和Transwell法检测VSMCs的增殖和迁移，流式细胞仪检测细胞凋亡。Targetscan数据库用于预测miR-637的靶基因。通过实时 PCR、蛋白质印迹和荧光素酶报告基因分析验证了 miR-637 和潜在靶基因之间的相互作用。MiR-637 在动脉粥样硬化患者和动物模型样品中的表达显着降低。在 ox-LDL 诱导的动脉粥样硬化动物模型中，它也以剂量和时间依赖性方式降低。转染 miR-637 模拟物可抑制 VSMC 的增殖和迁移，同时促进细胞凋亡，而转染 miR-637 抑制剂则具有相反的效果。我们还验证了胰岛素样生长因子-2 (IGF-2) 是动脉粥样硬化发病机制中的关键因素，可作为 miR-637 的靶基因。靶向 IGF-2 的 MiR-637 有助于抑制动脉粥样硬化，并可能成为该疾病的潜在靶点。转染 miR-637 模拟物可抑制 VSMC 的增殖和迁移，同时促进细胞凋亡，而转染 miR-637 抑制剂则具有相反的效果。我们还验证了胰岛素样生长因子-2 (IGF-2) 是动脉粥样硬化发病机制中的关键因素，可作为 miR-637 的靶基因。靶向 IGF-2 的 MiR-637 有助于抑制动脉粥样硬化，并可能成为该疾病的潜在靶点。转染 miR-637 模拟物可抑制 VSMC 的增殖和迁移，同时促进细胞凋亡，而转染 miR-637 抑制剂则具有相反的效果。我们还验证了胰岛素样生长因子-2 (IGF-2) 是动脉粥样硬化发病机制中的关键因素，可作为 miR-637 的靶基因。靶向 IGF-2 的 MiR-637 有助于抑制动脉粥样硬化，并可能成为该疾病的潜在靶点。