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由METTL14介导的lncRNA-FAS-AS1通过调节ADAM8的上升来促进骨关节炎的进展

Zhehua Zhang¹, Honggang Mao¹, Fang Li²

¹Department of Orthopedics, The Third Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia BaoGang Hospital, Baotou, Inner Mongolia, China.

International journal of rheumatic diseases

|September 2, 2024

概括

长非编码RNA FAS-AS1通过FMR1稳定ADAM8,激活JAK/STAT3通路,促进骨关节炎 (OA). METTL14调节FAS-AS1,影响OA的进展.

科学领域:

生物化学生化学
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

骨关节炎 (OA) 是一种广泛的退行性关节疾病.
长非编码RNAs (lncRNAs) 在OA病变发生中的作用是一个正在积极研究的领域.
了解像lncRNA-FAS-AS1这样的lncRNAs的调节机制对于开发新型OA疗法至关重要.

研究的目的:

在骨关节炎进展中研究lncRNA-FAS-AS1的功能和调节机制.
阐明涉及OA中FAS-AS1,FMR1和ADAM8的分子相互作用.
探索METTL14对FAS-AS1的上游调节及其对JAK/STAT3信号通路的影响.

主要方法:

通过使用IL-1β治疗的人类冠状细胞和OA动物模型建立了OA细胞模型.
通过RT-qPCR和Western blot评估基因和蛋白质的表达.
量化细胞活力,细胞亡和软骨损伤.
使用MeRIP研究了FAS-AS1的m6A修改.
使用RIP和RNA拉下测试确定了分子相互作用.

主要成果:

在OA模型中,FAS-AS1,METTL14和ADAM8得到了上调,以及激活的JAK/STAT3信号.
抑制FAS-AS1降低了细胞外基质的降解,这种效应被ADAM8过度表达所逆转.
通过招募FMR1.1,FAS-AS1稳定了ADAM8的mRNA.
在METTL14 Knockdown中,FAS-AS1的表达以一种m6A依赖的方式下降.
过度表达FAS-AS1抵消了METTL14对JAK/STAT3信号和软骨损伤的抑制作用.

结论:

通过METTL14调节的FAS-AS1促进了OA的进展.
FAS-AS1/FMR1/ADAM8轴激活了JAK/STAT3信号通路,有助于关节炎的发生.
准METTL14-FAS-AS1通路可能为骨关节炎提供治疗策略.

关键词:

在 ADAM8 中,在FAS-AS1中.FMR1 FMR1 的使用情况.在METTL14中,使用的是METTL14 骨关节炎是一种关节炎.

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