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沉默METTL3会增加HSP70的表达,并缓解角质细胞中的纤维化

Yapeng Jing^1,2, Jun Li³, Peng Hao³

¹School of Medicine, Nankai University, Tianjin, China.

Investigative ophthalmology & visual science

|November 6, 2024

概括

N6-甲基氨酸 (m6A) 修饰和METTL3在角膜纤维化中起作用. METTL3调节热冲击蛋白70 (HSP70) 的表达,影响纤维化发展,YTHDF2参与.

科学领域:

眼科医生眼科眼科
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.

背景情况:

角膜纤维化是视力障碍的重要原因之一.
N6-甲基氨酸 (m6A) 是一种表观遗传修饰,涉及到各种生物过程.
在角膜纤维化中m6A调节者的作用仍然在很大程度上未被探索.

研究的目的:

研究m6A及其调节器在角膜纤维化中的功能.
阐明基于m6A介导的角膜纤维化调节的机制.

主要方法:

在C57BL/6小鼠中的角膜烧模型和体外转化生长因子β1 (TGF-β1) 刺激的角质细胞.
使用siRNA对YTHDF2,METTL3和FTO进行基因沉默.
基因表达的定量分析通过qRT-PCR,西部涂抹和免疫组织化学.

主要成果:

m6A修饰和METTL3/FTO水平在角膜烧后和TGF-β1刺激时增加.
通过对METTL3和YTHDF2的沉默,提高了HSP70和减少了纤维化标志物的调节.
FTO静音对HSP70或纤维化没有显著影响.

结论:

METTL3参与调节角膜纤维化.
METTL3通过控制HSP70表达来调节角膜纤维化.
YTHDF2对于METTL3介导的角膜纤维化调节至关重要.

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