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尼古丁通过LINC01272/miR-515/KLF6轴诱导巨细胞灭

Lianjie Hou¹, Qin He², Yu Wang¹

¹The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan City People's Hospital, Qingyuan 511518, Guangdong, China.

Ecotoxicology and environmental safety

|July 21, 2023

概括

尼古丁会诱导巨细胞灭,这是动脉样硬化的关键过程. 这项研究显示,LINC01272通过海绵化miR-515来促进这种作用,从而增加KLF6表达和细胞死亡.

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
在RNA生物学,RNA生物学.

背景情况:

尼古丁是动脉样硬化的主要危险因素.
巨细胞是动脉样硬化斑块发展的核心.
长非编码RNAs (lncRNAs) 调节细胞功能,但它们在尼古丁诱导的巨细胞灭中的作用尚不清楚.

研究的目的:

调查 lncRNAs 在尼古丁诱导的巨细胞灭中的作用和机制.
为了识别参与这个过程的特定 lncRNA.

主要方法:

在人动脉斑块中选差异表达的lncRNAs.
在尼古丁处理的巨细胞中进行验证.
生物信息学分析,双 luciferase 记者基因测定和 qPCR.
免疫光染色. 免疫光染色.

主要成果:

确定LINC01272在尼古丁治疗的巨细胞中显著上调,以剂量依赖的方式.
与LINC01272的干扰抑制了尼古丁诱导的巨细胞灭.
发现LINC01272/miR-515/KLF6轴可以调解尼古丁诱导的巨细胞灭.
在吸烟者的外周血液单核细胞中观察到LINC01272和KLF6的增加和miR-515的减少.

结论:

尼古丁通过LINC01272/miR-515/KLF6轴促进巨细胞的灭.
LINC01272作为miR-515的分子海绵,缓解miR-515对KLF6.6的抑制作用.
这种机制有助于尼古丁诱导的动脉样硬化在吸烟者.

关键词:

巨细胞是一个巨细胞.尼古丁是一种尼古丁.没有编码的RNA.热灭菌的发生.烟草吸烟吸烟烟草吸烟

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