Department of Cardiology, The Second People's Hospital of Guiyang, Guiyang, Guizhou, China.
Department of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China.
Clin Hemorheol Microcirc. 2024;88(2):263-275. doi: 10.3233/CH-242261.
The precise association between lncRNA H19 and ferroptosis in the context of atherosclerosis remains uncertain.
This study is to clarify the underlying process and propose novel approaches for the advancement of therapeutic interventions targeting atherosclerosis.
Assessment of ferroptosis, which entails the evaluation of cell viability using CCK-8 and the quantification of intracellular MDA, GSH, and ferrous ions. Simultaneously, the protein expression levels of assessed by western blot analysis, while the expression level of lncRNA H19 was also determined. Furthermore, HAECs that were cultured with ox-LDL were subjected to Fer-1 interference. HAECs were exposed to ox-LDL and then transfected with H19 shRNA and H19 overexpression vector pcDNA3.1. The level of ferroptosis in the cells was then measured. Then, HAECs were subjected to incubation with ox-LDL, followed by transfection with H19 shRNA and treated with Erastin to assess the levels of ferroptosis, cell viability, and inflammatory factor production. and the ability for blood vessel development.
The survival rate of HAECs in the ox-LDL group was much lower. Ox-LDL resulted in an upregulation of ACSL4 expression in HAECs, while the expression of SLC7A11 and GPX4 decreased.
lncRNA H19 enhances ferroptosis and exacerbates arterial endothelial cell damage induced by LDL.
长链非编码 RNA H19 与动脉粥样硬化中的铁死亡之间的确切关联尚不清楚。
本研究旨在阐明潜在的过程，并提出针对动脉粥样硬化的治疗干预的新方法。
评估铁死亡，包括使用 CCK-8 评估细胞活力和定量细胞内 MDA、GSH 和亚铁离子。同时，通过 Western blot 分析评估蛋白质表达水平，同时测定 lncRNA H19 的表达水平。此外，用 Fer-1 干扰培养的 ox-LDL 的 HAEC。将 ox-LDL 暴露于 HAEC 中，然后转染 H19 shRNA 和 H19 过表达载体 pcDNA3.1。然后测量细胞中的铁死亡水平。然后，用 ox-LDL 孵育 HAEC，然后转染 H19 shRNA 并用 Erastin 处理，以评估铁死亡、细胞活力和炎症因子产生水平。和血管发育能力。
ox-LDL 组 HAEC 的存活率低得多。ox-LDL 导致 HAEC 中 ACSL4 表达上调，而 SLC7A11 和 GPX4 的表达下降。
lncRNA H19 增强了铁死亡，并加重了 LDL 诱导的动脉内皮细胞损伤。
