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c-JUN是hESC中阻碍心肌细胞过渡的障碍物

Hui Zhong^1,2, Ran Zhang^1,3,4, Guihuan Li³

¹Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.

Life science alliance

|August 21, 2023

概括

丢失c-JUN令人惊地增强了人类心肌细胞的生成,通过增加染色质的可访问性和H3K4me3沉积,揭示了心脏发育调节中的新角色.

科学领域:

发展生物学发展生物学
干细胞生物学干细胞生物学
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:

在小鼠中,c-JUN损失导致胚胎死亡,与心脏系统缺陷有关.
目前尚不清楚c-JUN在人类心肌细胞细胞命运决定中的作用.

研究的目的:

研究c-JUN在人体多能干细胞在体外分化成心肌细胞中的功能.
阐明c-JUN影响人类心脏发育的分子机制.

主要方法:

在体外分化人类多能干细胞 (hPSCs) 变成心肌细胞.
使用ATAC-seq.进行染色体可访问性分析.
使用ChIP-seq对H3K4me3.3进行质子修饰分析.
基因表达分析通过单细胞RNA-seq.
药理上抑制了组织素脱甲基酶活性.

主要成果:

敲除c-JUN显著改善了心肌细胞的产生,这可以通过增加TNNT2+细胞来证明.
c-JUN 缺乏导致了在关键心脏调节元件的增强色素可访问性.
c-JUN淘汰赛增加了RBBP5和SETD1B的表达,提高了心脏发生基因上的H3K4me3水平.
激素脱甲基酶的药理抑制模仿了c-JUN KO表型,增强了心肌细胞的产生.
单细胞RNA-seq显示,c-JUN淘汰激活了更多与心脏发生相关的规律子.

结论:

c-JUN 负面调节人类心肌细胞分化.
c-JUN通过调节H3K4me3表观遗传标记和染色质可访问性来控制心肌细胞命运.
这些发现为c-JUN在人类心脏发育中的作用提供了新的见解.

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