引言 动脉硬化闭塞症（ASO）是一种影响下肢的疾病。ASO的机制涉及血管平滑肌细胞（VSMCs）的增殖和迁移。miR-4284参与心血管系统中的多个生物学过程，包括VSMCs的增殖、迁移和死亡。然而，尚不清楚miR-4284基因是否参与ASO的调控。此外，人类动脉平滑肌细胞（HASMCs）作为动脉壁的重要组成部分，其对动脉硬化闭塞症（ASO）发病机制的贡献仍不清楚。我们之前研究了ASO患者血液中miRNA的变化，现在我们希望进一步测试这些变化是否也发生在负责ASO发病机制的HASMCs中。 方法 通过实时聚合酶链反应分析动脉壁中miR-29a的表达水平。建立ASO细胞模型以调查miR-4284对HASMCs的表达情况。采用Transwell系统和CCK-8检测评估HASMCs的迁移和增殖。通过流式细胞术评估凋亡细胞的比例以及凋亡信号蛋白产生的浓度。采用Western blot技术鉴定B细胞淋巴瘤-2（Bcl2）、Bcl2相关X蛋白（BAX）以及X联锁抑制剂蛋白（XIAP）。 结果 结果显示，PCR确认，在没有FBS和在1% O2 + 5% CO2 + 94% N2气氛下培养的HASMCs中，miR-4284的产物或表达显著降低，而葡萄糖对其表达无影响。miR-4284对迁移和增殖无影响，但miR-4284的下调可以降低HASMCs的凋亡率，流式细胞术显示。此外，Western blot实验显示BAX的表达较低，而另外两种蛋白Bcl2和XIAP的表达过度表达。 结论 我们发现，miR-4284的下调增强了Bcl2以及XIAP的表达，同时降低了BAX的表达。这表明下调的miR-4284调节了HASMCs中与凋亡相关的蛋白表达。该机制尚不清楚，需要进一步研究以确认。Copyright© Bentham Science Publishers；如有任何问题，请发送电子邮件至epub@benthamscience.net。

Introduction The disease arteriosclerosis obliterans (ASO) affects the lower extremities. ASO's mechanism involves the proliferation and migration of vascular smooth muscle cells (VSMCs). The miR-4284 is involved in several biological processes of the cardiovascular system, including VSMC proliferation, migration, and death. However, it is unknown if the miR-4284 gene is involved in the control of ASO. Furthermore, the molecular processes behind the contribution of human arterial smooth muscle cells (HASMCs), one of the most significant components of the arterial wall, to arteriosclerosis obliterans (ASO) pathogenesis remain unknown. Previously, we explored the alterations of miRNAs in the blood of ASO patients, and now we wanted to test further whether these changes also take place in the HASMCs that are responsible for the pathogenesis of ASO. Methods The expression levels of miR-29a in arterial walls were analyzed via a real-time polymerase chain reaction. An ASO cell model was established to investigate the expression of miR-4284 on HASMCs. The Transwell system and CCK-8 detection were used to assess the migration and proliferation of HASMCs. The proportion of apoptotic cells as well as the concentrations of apoptotic signal protein production were assessed using flow cytometry. A Western blot technique was used to identify B cell lymphoma-2 (Bcl2), Bcl2-associated X protein (BAX), as well as X-linked inhibitors of apoptosis protein (XIAP). Results The results showed that PCR confirmed that the qualified production or expression of miR-4284 was significantly reduced in HASMCs after they were cultured without FBS and in an atmosphere of 1% O2 + 5% CO2 + 94% N2 and that glucose had no effect on its expression. MiR-4284 has no effect on migration and proliferation, but downregulation of miR-4284 can decrease the apoptotic rate of HASMCs, as revealed by flow cytometry. Furthermore, western blot experiments showed that the expression of BAX was low, while the expression of the other two proteins, viz., Bcl2 and XIAP, was over-expressed. Conclusion We found that miR-4284 downregulation enhanced Bcl2, as well as XIAP, and decreased Bax. This shows that downregulated miR-4284 regulates apoptosis-related protein expression in HASMCs. The mechanism is not clear, and we need further study to confirm it.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.