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通过内皮细胞激活GPR4信号,GPRASP1功能丧失与动脉静脉形不全有关

Ruofei Li¹, Xiao Xiao¹, Yupeng Yan¹

¹State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.

Brain : a journal of neurology

|October 3, 2023

概括

在G蛋白结合受体相关排序蛋白1 (GPRASP1) 的遗传变异导致内皮功能障碍,导致动脉静脉形 (AVMs) 和脑出血. 针对GPR4和JNK通路的治疗策略显示出治疗这些血管疾病的前景.

科学领域:

遗传学和分子生物学
血管生物学血管生物学
细胞信号传输细胞信号传输

背景情况:

动脉静脉形 (AVM) 是年轻成年人脑内出血的重要原因.
了解AVM的遗传基础对于开发有效的治疗方法至关重要.
在血管发育中的G蛋白结合受体 (GPCR) 相关排序蛋白1 (GPRASP1) 功能基本上是未知的.

研究的目的:

研究GPRASP1在AVM病变发生中的作用.
识别与AVM相关的遗传变异及其功能后果.
阐明了GPRASP1介导的内皮功能障碍背后的分子机制.

主要方法:

在AVM患者中识别和功能验证GPRASP1误解变异.
在体外和体内研究使用内皮细胞和Gprasp1淘汰小鼠.
分析GPR4信号通路,无处不在和内分泌体贩运.

主要成果:

在AVM患者中,在GPRASP1中发现了新的功能丧失变异.
在小鼠中,GPRASP1缺乏导致内皮功能障碍,脑出血,AVM和多器官血管异常.
删除GPRASP1通过防止GPR4降解来激活GPR4/cAMP/MAPK信号,从而导致血管缺陷.

结论:

GPRASP1在维持内皮功能和预防AVM发展方面发挥着至关重要的作用.
GPRASP1调节GPR4的稳定性和信号传输,影响血管平衡.
准GPR4和JNK通路为AVM提供了潜在的治疗策略.

关键词:

在 GPR4 中使用.这就是GPRASP1的基本规则.这是一种动脉静脉形形.降解降解降解降解降解.细胞内皮细胞的内皮细胞.

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