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根据BCL6B抑制ETV2,阻碍内皮细胞分化

Zhonghao Li¹, Wei Wu², Qiushi Li¹

¹Department of Cardiology, Translational Research Center for Regenerative Medicine and 3D Printing Technologies, Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510150, China.

Stem cell research & therapy

|July 29, 2024

概括

B细胞CLL/淋巴瘤6成员B (BCL6B) 通过抑制ETV2来抑制内皮细胞 (EC) 分化. 这一发现揭示了调节血管发育的新机制,并提供了潜在的治疗点.

科学领域:

分子生物学分子生物学
干细胞生物学干细胞生物学
血管生物学血管生物学

背景情况:

BCL6B是一种转录抑制剂,参与各种细胞过程.
它在内皮细胞 (EC) 发育中的作用以前是未知的.
众所周知,ETV2是EC差异化的促进者.

研究的目的:

研究BCL6B在EC分化中的作用.
阐明BCL6B在EC发育中的作用的基本机制.

主要方法:

在人类诱导多能干细胞 (hiPSCs) 中,BCL6B的过度表达和敲除.
基因表达和差异化效率的RNA测序,qRT-PCR和流细胞计.
试管培养试验和免疫光检测用于EC功能和结构.
路西法酶报告器和ChIP-PCR测定以确定BCL6B-ETV2相互作用.

主要成果:

过度表达BCL6B抑制了来自hiPSCs的EC分化和管形成.
在BCL6B的淘汰下,改善了EC的差异化.
BCL6B直接与ETV2促进体结合,抑制其转录活性.
过度表达ETV2挽救了BCL6B的抑制作用.

结论:

BCL6B抑制了EC分化和血管有机体的发展.
这种抑制通过抑制ETV2转录活性而发生.
BCL6B代表了血管发育的新型调节者.

关键词:

B细胞CLL/淋巴瘤6成员B成员排放交易系统变种转录因子2 内皮细胞内皮细胞的内皮细胞.人类诱导的多能干细胞干细胞.船舶的器官类动物.

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