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环ZNF609海绵miR-135b对SEMA3A的表达进行上调,以缓解ox-LDL诱导的动脉样硬化

Jian Hou¹, Lingling Zheng², Xiangyun Li³

¹Department of Cardiology, The Second Affiliated Hospital of Shandong First Medical University, No. 366, Taishan Street, Tai'an, 271021, Shandong, People's Republic of China.

Molecular and cellular biochemistry

|May 31, 2024

概括

循环RNA ZNF609 (circZNF609) 的过度表达通过降低miR-135b的调节和提高SEMA3A (SEMA3A) 的调节来减轻动脉样硬化,减少脂质积累和炎症.

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
生物化学生物化学

背景情况:

动脉样硬化 (AS) 的发病包括异常的脂质代谢和脂质滴滴积累.
在AS患者中,MicroRNA-135b (miR-135b) 的上调,与SEMA3A和circZNF609水平相反相关.

研究的目的:

研究circZNF609在缓解AS进展中的作用.
阐明AS中涉及miR-135b和SEMA3A的分子机制.

主要方法:

在体外AS模型使用ox-LDL刺激的U937巨细胞.
在体内AS小鼠模型.
这些测试包括ORO,ELISA,RT-qPCR,西部斑,JC-1,FCM,RIP,HE染色和IHC.

主要成果:

过度表达circZNF609减少了脂质积累,炎症,线粒体功能障碍和细胞死亡.
circZNF609直接与miR-135b结合,而circZNF609的过度表达可以调节SEMA3A.
抑制miR-135b或过度表达circZNF609/SEMA3A挽救了与AS相关的损伤.
在体内,circZNF609/SEMA3A过度表达逆转了AS的进展.

结论:

过度表达的circZNF609通过消耗miR-135b和上调SEMA3A.抑制AS进展.
这种机制减轻了AS模型中的脂质积累,线粒体功能障碍和细胞死亡.

关键词:

动脉样硬化是一种动脉样硬化.脂质的积累脂质的积累线粒体功能障碍线粒体功能障碍氧-LDL是一种LDL.塞马福林 3A 种类 circZNF6099 的时间在 miR-135bb 中使用.

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