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lncRNA GAPLINC调节了动脉样硬化中的血管内皮细胞亡

Jun Pan¹, Bing Wang¹, Xibin Pu^1,2

¹Department of Vascular Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Archives of medical science : AMS

|February 28, 2024

概括

这项研究表明,长非编码RNA GAPLINC,当被氧化低密度脂蛋白 (ox-LDL) 上调时,会抑制内皮细胞的增殖. GAPLINC通过隔离miR-183-5p来实现这一目标,从而增加PDCD4表达和亡.

科学领域:

分子生物学分子生物学
心血管研究研究心血管研究
在RNA生物学,RNA生物学.

背景情况:

动脉样硬化是一种由脂质积累和内皮功能障碍驱动的慢性炎症性疾病.
长非编码RNAs (lncRNAs) 越来越多地被认为是它们在调节与心血管疾病相关的细胞过程中的作用.
氧化低密度脂蛋白 (ox-LDL) 是动脉样硬化开始和进展的关键因素.

研究的目的:

为了研究 lncRNA GAPLINC 在暴露于ox-LDL的内皮细胞中的作用.
阐明GAPLINC影响细胞对ox-LDL的反应的分子机制.

主要方法:

人类大动脉内皮细胞 (HAEC) 用ox-LDL进行了治疗.
使用定量PCR (qPCR) 来测量GAPLINC表达.
流细胞计和TUNEL试验评估了细胞亡和细胞循环.
路西法雷斯记者测定和西布洛特证实了分子相互作用.

主要成果:

氧化低密度脂蛋白 (ox-LDL) 治疗在HAEC中调高了GAPLINC表达.
过度表达GAPLINC抑制了细胞增殖,诱导了细胞亡,并导致细胞循环停止.
GAPLINC作为miR-183-5p的分子海绵,阻止它准PDCD4.
这导致PDCD4表达的增加以及随后的细胞效应.

结论:

在 lncRNA GAPLINC 的上调促进了 PDCD4 的表达,通过隔离 miR-183-5p.
这种机制有助于ox-LDL诱导的内皮细胞亡和抑制增殖.
GAPLINC在细胞对ox-LDL的反应中发挥着重要作用,使其成为动脉样硬化中的潜在治疗标.

关键词:

盖普林斯 (GAPLINC) 的时间动脉样硬化动脉样硬化细胞亡是细胞的亡.长非编码RNA是什么意思 ox-LDL 的使用情况.

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