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ETV2通过转录激活Rig1基因表达,并促进内皮细胞系的重编程

Young Geun Choi^1,2, Xiao Ma^1,2, Satyabrata Das^1,2

¹Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, MN, 55455, USA.

Scientific reports

|November 20, 2024

概括

ETV2 (Ets变体2) 直接激活RIG1 (Ripk1-交互的Golgi蛋白1),将纤维细胞重新编程成内皮细胞. 这一发现澄清了潜在的重血管化疗法的机制.

科学领域:

分子生物学分子生物学
发育生物学是发展生物学.
细胞生物学细胞生物学

背景情况:

ETV2 (Ets变体2) 是胚胎血管发育必不可少的关键转录因子.
ETV2充当先驱因素,能够直接将体细胞 (如纤维细胞) 重编程为内皮细胞.
控制ETV2介导细胞重编程的精确分子机制尚未完全理解.

研究的目的:

研究ETV2介导的纤维细胞转化为内皮细胞的分子机制.
确定参与这种细胞转化过程的关键调节途径.

主要方法:

在小鼠胚胎纤维细胞 (MEF) 中利用可诱导的ETV2表达系统.
使用单细胞RNA测序 (scRNA-seq) 来分析重编程期间的转录变化.
进行了ChIP-seq,电泳运动转移试验 (EMSA) 和转录试验,以研究基因调节.
使用shRNA来击败Rig1和Nfκb1的表达.

主要成果:

scRNA-seq揭示了与Rig1-like受体信号通路相关的转录网络的诱导.
ETV2被确定为Rig1基因表达的直接上游激活剂.
敲除Rig1或Nfκb1显著降低了内皮细胞重编程的效率.

结论:

ETV2主要通过直接激活RIG1.1,将纤维细胞重新编程为内皮细胞.
这项研究阐明了细胞重编程中的关键ETV2-RIG1信号级联.
研究结果为开发对缺血性疾病的重血管化策略提供了洞察力.

关键词:

在 ETV2 上播放.在RIG1中,RIG1是指RIG1.重编程重编程是一种重编程.

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