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形成动脉样硬化的表观遗传特征

Paul Cheng¹, Robert C Wirka², Lee Shoa Clarke¹

¹Division of Cardiovascular Medicine and the Cardiovascular Institute, Stanford, CA (P.C., L.S.C., Q.Z., R.K., T.N., D.S., H.-j.K., H.S., T.A., J.B.K., T.Q.).

|January 6, 2022

概括

在动脉样硬化过程中,转录因子ZEB2在平滑的肌肉细胞转换中起着至关重要的作用. 通过调节血管细胞的表观遗传变化,针对ZEB2提供了冠状动脉疾病 (CAD) 的新疗法.

科学领域:

心血管生物学
表观遗传学
分子医学

背景情况:

在动脉样硬化中,光滑肌细胞 (SMC) 采用多种表型,形成大部分斑块细胞.
了解这些细胞状态变化的表观遗传和转录调节对于冠状动脉疾病 (CAD) 风险至关重要.

研究的目的:

调查2q22.3的复杂CAD全基因组关联研究信号的因果基因和细胞机制.
阐明相关位置的转录因子如何影响SMC表型和CAD风险.

主要方法:

使用CRISPR-Cas9基因组和表观基因组编辑来确定因果基因和调节元素.
在小鼠模型和人类SMC中采用单细胞表观遗传和转录基因分析.
研究了转录因子ZEB2在SMC表型转换中的功能.

主要成果:

在2q22.3的CAD遗传信号位于ZEB2转录因子的光滑肌肉增强剂内.
ZEB2通过染色体重塑来调节SMC过渡,影响Notch和TGF-β信号.
损失ZEB2损害了SMC过渡到类似纤维细胞的状态,但加速了冠状肌细胞的形成,模仿了高风险斑块.

结论:

通过直接的表观遗传影响,ZEB2被确定为一种新的CAD风险基因.
针对ZEB2为血管疾病提供了新的治疗途径.

关键词:

动脉样硬化表观基因组遗传学肌肉,光滑的

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