在内皮细胞中,ZO-1 与YB-1 相互作用,以调节血管生成过程中压力颗粒的形成
Yassine El Bakkouri1, Rony Chidiac1,2, Chantal Delisle1
1Department of Pharmacology and Physiology, Faculty of Medicine, Université de Montréal, Montreal, Quebec, Canada.
Nature communications
|May 23, 2024
概括
Zonula occludens-1 (ZO-1) 蛋白降低调节增强了内皮细胞的压力颗粒形成,保护细胞免受损伤. 这种与Y盒结合蛋白1 (YB-1) 的相互作用对血管生成和细胞应激反应至关重要.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 血管生物学 血管生物学
背景情况:
- 佐努拉闭塞-1 (ZO-1) 调节内皮细胞 (EC) 结.
- 压力颗粒 (SG) 是细胞质焦点,在细胞压力下形成.
研究的目的:
- 为了识别ZO-1蛋白互动组.
- 调查ZO-1在血管新生过程中SG形成和EC应激反应中的作用.
主要方法:
- 蛋白质组学用于识别ZO-1相互作用蛋白.
- 在EC中进行细胞应力测试 (例如,酸盐治疗).
- 在体内研究使用内皮特异性的ZO-1淘汰赛小鼠.
主要成果:
- ZO-1 与压力颗粒中的RNA结合蛋白相互作用,包括Y盒结合蛋白1 (YB-1).
- 降低ZO-1的调节增加了SG的形成,并赋予了细胞保护.
- 在小鼠中,内皮特异性的ZO-1缺失破坏了视网膜血管生成,并改变了EC形态.
结论:
- ZO-1通过与YB-1的相互作用来调节SG的形成.
- 这一法规影响了欧盟的应激反应和血管生成.
- 向ZO-1-YB-1相互作用可能为血管疾病提供治疗潜力.
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