通过 miR-673-5p/TFRC 轴敲除 circSlc8a1 可抑制血管紧张素 II 处理的 H9c2 细胞的铁卟啉沉积作用

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Kaidi Wu, Jiawei Du
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引用次数: 0

摘要

背景本研究旨在探讨circSlc8a1在心肌肥厚(CH)中的作用,心肌肥厚是多种心血管疾病的一种病理变化。方法使用血管紧张素II(AngII)处理的H9c2细胞建立体外CH模型,然后进行Western印迹和RT-qPCR检测相对表达。细胞活力和增殖采用 CCK-8 和 EdU 检测法进行分析,乳酸脱氢酶(LDH)、活性氧(ROS)、谷胱甘肽(GSH)和铁水平则采用相应的试剂盒进行测定。结果表明,在 AngII 处理的 H9c2 细胞中,circSlc8a1 和 TFRC 的表达量增加,而 miR-673-5p 的表达量减少。铁变态反应抑制剂处理降低了心房利钠肽(ANP)、脑利钠肽(BNP)、β-主要组织相容性复合体(β-MHC)蛋白的表达和circSlc8a1的表达。敲除 circSlc8a1 可抑制细胞活力和增殖,增加 GSH 含量、谷胱甘肽过氧化物酶 4 和溶质运载家族 7 成员 11 蛋白表达,降低 LDH、ROS、铁水平和 RAS 蛋白表达。MiR-673-5p 抑制剂拮抗了 si-circSlc8a1 的作用,过表达的 TFRC 逆转了 AngII 处理的 H9c2 细胞的 miR-673-5p 模拟效应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Knockdown of circSlc8a1 inhibited the ferroptosis in the angiotensin II treated H9c2 cells via miR-673-5p/TFRC axis

Knockdown of circSlc8a1 inhibited the ferroptosis in the angiotensin II treated H9c2 cells via miR-673-5p/TFRC axis

Background

This study aimed to investigate the role of circSlc8a1 in cardiac hypertrophy (CH), a pathological change in various cardiovascular diseases.

Methods

An in vitro CH model was established using angiotensin II (AngII) treated H9c2 cells, followed by western blotting and RT-qPCR for detecting relative expressions. Cell viability and proliferation were analyzed using CCK-8 and EdU assays, while lactate dehydrogenase (LDH), reactive oxygen species (ROS), glutathione (GSH), and iron levels were determined using corresponding kits. Moreover, dual-luciferase reporter and RNA pull-down assays were performed to demonstrate whether miR-673-5p is bound to circSlc8a1 or transferrin receptor (TFRC).

Results

The results indicated that the expressions of circSlc8a1 and TFRC were increased, while miR-673-5p was decreased in the AngII treated H9c2 cells. The ferroptosis inhibitor treatment decreased the atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and β-major histocompatibility complex (β-MHC) protein expressions, and circSlc8a1 expressions. Knocking down of circSlc8a1 inhibited promoted the cell viability and proliferation, increased the GSH content, glutathione peroxidase 4, and solute carrier family 7 member 11 protein expressions, and decreased the LDH, ROS, iron levels, and RAS protein expressions. The MiR-673-5p inhibitor antagonized the role of si-circSlc8a1, and the over-expressed TFRC reversed the miR-673-5p mimicking effects in AngII treated H9c2 cells.

Conclusion

CircSlc8a1 promoted the ferroptosis in CH via regulating the miR-673-5p/TFRC axis.

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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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