NONHSAT098487.2通过调节Notch通路来保护心肌细胞免受氧化应激损伤
Guiju Feng1, Hong Zhang1, Qingling Guo2
1Department of General Practice, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China.
Heliyon
|July 6, 2023
概括
一种新的长非编码RNA,NONHSAT098487.2,可以保护心脏细胞免受氧化应激. 这种RNA在急性心肌梗塞患者中被上调,并激活了Notch通路,为心脏损伤提供了潜在的治疗点.
科学领域:
- 心血管生物学 心血管生物学
- 分子心脏病学分子心脏病学
- 非编码RNA研究研究
背景情况:
- 急性心肌梗塞 (AMI) 是全球心血管死亡的主要原因.
- 长非编码RNAs (lncRNAs) 与心血管疾病有关,但它们在保护心肌细胞免受氧化压力的作用尚不清楚.
- 反应性氧物种 (ROS) 在AMI中对心肌细胞损伤有显著的贡献.
研究的目的:
- 研究新型lncRNA NONHSAT098487.2在保护心肌细胞免受过氧化 (H2O2) 诱导的氧化应激作用中的功能.
- 探索涉及Notch信号通路的潜在分子机制.
主要方法:
- 定量实时聚合酶链反应 (qRT-PCR) 用于基因表达分析.
- 细胞活力测试 (细胞计数套件-8),乳酸脱酶 (LDH) 释放测试,以及用于评估亡的流细胞计量.
- 西部涂抹以评估蛋白质水平和Notch通路激活. 使用隙抑制剂 (DAPT) 来确认途径的参与.
主要成果:
- 在AMI患者的外周血液单核细胞中,NONHSAT098487.2表达升高,与心脏损伤生物标志物 (HS-TnT,CK-MB) 相相关.
- NONHSAT098487.2在氧化应激 (H2O2) 或低氧/低氧化状态下在心肌细胞上调调.
- Knockdown 的 NONHSAT098487.2 通过抑制 Notch 信号来加剧 H2O2 诱导的损伤,而它的过度表达通过激活 Notch 信号来保护细胞.
结论:
- 在心肌细胞中,lncRNA NONHSAT098487.2 证明了对氧化应激的保护作用.
- NONHSAT098487.2通过调节Notch信号通路来发挥其保护作用.
- 这种新型的lncRNA代表了缓解急性心肌梗塞等疾病中心肌细胞损伤的潜在治疗标.
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