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通过 AMIGO2 的 m6 A-YTHDC2 介导调节,METTL3 淘汰抑制 RA-FLS 激活

Tingyu Miao¹, Yue Qiu¹, Jing Chen¹

¹Department of Cell Biology, School of Medicine, Yangzhou University, Yangzhou 215000, China.

Biochimica et biophysica acta. Molecular basis of disease

|March 3, 2024

概括

甲基转移酶类3 (METTL3) 通过影响粘附分子与Ig类域2 (AMIGO2) 表达来调节类风湿性关节炎纤维细胞类同胞细胞 (RA-FLS). 沉默METTL3通过m6A-YTHDC2-AMIGO2通路抑制RA-FLS的扩散和攻击.

科学领域:

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.
类风湿病学类风湿病学

背景情况:

N6-甲基氨酸 (m6A) 的mRNA失调有助于类风湿性关节炎 (RA) 的发病.
甲基转移酶类3 (METTL3) 是一个关键的m6A甲基转移酶,在RA组织和细胞中被上调.

研究的目的:

调查METTL3介导的m6A修饰在RA纤维细胞样同胞细胞 (RA-FLS) 中的作用.
确定RA-FLS中METTL3的下游目标和分子机制.

主要方法:

在RA-FLS中抑制METTL3.
确定AMIGO2作为下游目标.
在AMIGO2 mRNA 5'-未翻译区域 (5'UTR) 中分析m6A修饰.
评估METTL3-YTHDC2与AMIGO2mRNA的相互作用.

主要成果:

消除METTL3减少了RA-FLS的扩散,迁移和入侵.
具有Ig类似域2 (AMIGO2) 的粘附分子被确定为METTL3和YTHDC2.2的标.
降低了AMIGO2mRNA5'UTR中的m6A修饰,减少了YTHDC2相互作用.
过度表达AMIGO2可以逆转METTL3或YTHDC2 knockdown的表型效应.

结论:

通过降低AMIGO2.2的调节,METTL3静音抑制RA-FLS的扩散和攻击性行为.
METTL3-m6A-YTHDC2-AMIGO2轴在调节RA-FLS表型方面发挥着至关重要的作用.
这一途径代表了类风湿性关节炎的潜在治疗标.

关键词:

粘附分子与Ig类似域2的粘附分子.类似于甲基转移酶的3 N(6) - - 甲基氨酸.类风湿性关节炎纤维细胞样同胞细胞.包含2个内容的YTH域名

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