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通过LncRNA H19-EZH2相互作用,通过重编程H3K27me3配置文件,促进肝纤维化

Xiao-Jiao-Yang Li¹, Fei Zhou², Ya-Jing Li²

¹School of Life Sciences, Beijing University of Chinese Medicine, Beijing, 100029, China. xiaojiaoyang.li@bucm.edu.cn.

Acta pharmacologica Sinica

|August 14, 2023

概括

高表达的长非编码RNAH19通过重编程EZH2介导的肝星细胞表观遗传调节来促进肝纤维化. 准H19-EZH2相互作用为肝纤维化提供了一个新的治疗策略.

科学领域:

肝病学肝病学是一种肝病学.
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
分子生物学分子生物学

背景情况:

肝纤维化涉及过度的细胞外基质沉积,由激活的肝星细胞 (HSC) 驱动.
EZH2 (表观遗传调节器) 和长非编码RNA H19 都与纤维生成有关.
在肝纤维化中连接H19,EZH2和HSC激活的精确机制尚未完全阐明.

研究的目的:

调查H19和EZH2导致肝纤维化的潜在机制.
在肝纤维化模型中探索向H19-EZH2相互作用的治疗潜力.

主要方法:

使用了各种肝纤维化的小鼠模型 (Mdr2^-/-,BDL,CCl_4).
服用EZH2抑制剂 (3-DZNeP,GSK126) 以评估它们对HSC和纤维化模型的影响.
使用RNA-pull-down,RNA免疫沉,RNA-sequencing (RNA-seq) 和ChIP-sequencing (ChIP-seq) 来分析分子相互作用和表观遗传修饰.

主要成果:

在肝纤维化模型中,EZH2被上调,与H19和纤维化标志物相关联.
在体内,EZH2抑制显示出显著的保护作用.
H19直接与EZH2结合,重新编程EZH2介导的H3K27me3配置文件.
这种表观遗传重编程通过EMT和Wnt/β-catenin信号传递等途径促进HSC激活和扩散.

结论:

慢性肝病中的过度表达的H19通过通过EZH2.2.通过表观遗传调节HSC激活来驱动纤维化.
H19-EZH2相互作用是肝纤维化的关键媒介.
针对H19-EZH2相互作用,为肝纤维化提供了一个有前途的新疗法策略.

关键词:

这是一个3-DZNeP.在 EZH2 中使用.H19 H19 是一种H19病毒.表观遗传调节表观遗传调节肝脏纤维化肝脏纤维化文素 (Quercetin) 是一种文素.

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