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在动脉样硬化中,NKILA与一些亡基因表达之间的关联

Burcu Bayyurt¹, Şeyda Akın¹, Nil Özbilüm Şahin²

¹Department of Medical Biology, Faculty of Medicine, Sivas Cumhuriyet University, Sivas, Turkey.

|August 26, 2024

概括

这项研究表明,长非编码RNANKILA可以通过减少内皮细胞亡来预防动脉样硬化. 在用氧化LDL治疗的细胞中抑制NKILA增加了亲亡基因的表达,这表明NKILA.

科学领域:

心血管生物学心血管生物学
分子生物学分子生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

氧化低密度脂蛋白 (ox-LDL) 诱导内皮功能障碍和亡,这是动脉样硬化发展的关键因素.
长非编码RNAs (lncRNAs) 越来越多地被认为是它们在血管生物学和心血管疾病 (CVD) 中的作用.
已知NF-κB相互作用的lncRNA (NKILA) 抑制NF-κB信号传递,这是一种涉及到ox-LDL诱导的内皮损伤的途径.

研究的目的:

在动脉样硬化背景下调查NKILA在调节内皮细胞 (EC) 亡中的作用.
测试NKILA影响EC亡并导致动脉样硬化病变的假设.

主要方法:

使用定量逆转录聚合酶链反应 (RT-qPCR) 来分析基因表达.
人类静脉内皮细胞 (HUVECs) 用ox-LDL进行治疗,并用NKILA siRNA感染.
测量了与亡相关的基因 (BAX,CASP9,CYCS,APAF1,BCL-2) 的表达水平.

主要成果:

用牛-LDL和NKILA siRNA治疗导致HUVECs中BAX,CASP9,CYCS,APAF1和BCL-2基因表达的下调.
在增加NKILA基因表达和增加BAX,CASP9,APAF1和BCL-2的表达之间观察到显著的正相关性.

结论:

通过调节EC亡,NKILA可能在动脉样硬化中发挥保护作用.
在NKILA沉默后的基因表达分析提供了关于动脉样硬化中EC亡的表观遗传调节的见解.
对动脉样硬化中EC亡的进一步表观遗传学研究可以从这些发现中受益.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.动脉样硬化是一种动脉样硬化.内皮细胞内皮细胞的内皮细胞.基因表达基因表达基因表达尼基拉 (NKILA) 是一个

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