长非编码RNAFKSG29调节氧化应激和内皮功能障碍在阻塞性睡眠呼吸暂停
Yung-Che Chen1,2,3, Po-Yuan Hsu4, Mao-Chang Su4,5,6
1Division of Pulmonary and Critical Care Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung City, Taiwan. yungchechen@yahoo.com.tw.
Molecular and cellular biochemistry
|November 2, 2023
概括
这项研究确定了长非编码RNAFKSG29作为阻塞性睡眠呼吸暂停 (OSA) 相关的内皮功能障碍的关键参与者. 准FKSG29及其相关的微RNA通路为OSA并发症提供了潜在的新疗法.
科学领域:
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
- 心血管研究研究心血管研究
背景情况:
- 阻塞性睡眠呼吸暂停 (OSA) 与内皮功能障碍有关,部分原因是改变了亲/抗氧化剂基因表达.
- 间歇性低氧与再氧化 (IHR) 是OSA病理生理学的标志,诱导细胞应激和功能障碍.
研究的目的:
- 调查新型长非编码RNA (lncRNA) FKSG29在OSA中IHR诱导的内皮功能障碍中的作用.
- 探索涉及FKSG29,microRNA-23a-3p和下游目标在OSA相关的内皮损伤中的调节机制.
主要方法:
- 对OSA患者和对照者的外周血液单核细胞中FKSG29,氧化应激标记物和血管活性基因的基因表达分析.
- 在体外研究中,使用暴露于IHR的THP-1和HUVEC细胞,涉及基因淘汰/淘汰和双露西法酶记者分析.
- 免疫光染色以评估细胞吸收和信号通路激活.
主要成果:
- 在OSA患者中,FKSG29 lncRNA,NOX2,NOX5和VEGFA被上调,而SOD2和VEGFB被下调.
- 在实验室中,FKSG29的淘汰改善了IHR诱导的氧化应激,亡和改变的基因表达,这种效应取决于miR-23a-3p.
- FKSG29充当miR-23a-3p的海绵,调节IL6R和下游炎症/内皮激活标记物 (ICAM1,VCAM1).
结论:
- 通过miR-23a-3p/IL6R轴,FKSG29在OSA中介于IHR诱导的内皮功能障碍方面发挥着关键作用.
- 针对FKSG29和相关途径的组合RNA干扰为OSA相关的内皮功能障碍提供了潜在的治疗策略.
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