线粒体基于HUR/PIM1信号通路在高血压血管内皮细胞损伤中的机制

doi:10.3969/j.issn.1006⁃5725.2022.24.004

实用医学杂志 ›› 2022, Vol. 38 ›› Issue (24): 3043-3048.doi: 10.3969/j.issn.1006⁃5725.2022.24.004

线粒体基于HUR/PIM1信号通路在高血压血管内皮细胞损伤中的机制

尹磊蒋志明杨慧琼刘燕飞郑学斌

长沙市第四医院心血管二科（长沙 410000）

出版日期:2022-12-25 发布日期:2022-12-25
通讯作者: 蒋志明 E⁃mail：fwtk2576732@163.com
基金资助:
湖南省卫生健康委员会科研课题（编号：20200124）

Mechanism of mitochondria⁃based HUR/PIM1 signaling pathway in hypertensive vascular endothelial cell injury

YIN Lei，JIANG Zhiming，YANG Huiqiong，LIU Yanfei，ZHENG Xuebin.

Department of Cardiology，the Fourth Hospital of Changsha，Changsha 410000，China

Online:2022-12-25 Published:2022-12-25
Contact: JIANG Zhiming E⁃mail：fwtk2576732@163.com

摘要/Abstract

摘要：

目的基于 HUR/PIM1 信号通路探讨线粒体在高血压血管内皮细胞损伤中的机制。方法 AngⅡ处理人脐血管内皮细胞（HUVCE）分为 3 组：control 组、AngⅡ组和 Mdivi⁃1 组。CCK⁃8、流式细胞术和 transwell 检测细胞活力、凋亡及迁移率。线粒体选择性探针检测线粒体形态，JC⁃1 染料测量线粒体膜电位。qPCR 和 Western blot 检测细胞中 Drp⁃1、ROS、HUR/PIM1 mRNA 和蛋白含量，体外血管形成验证血管生成。结果与 control 组比较，AngⅡ组细胞活力降低、Drp⁃1 和 ROS 蛋白表达升高和线粒体形态改变及膜电位降低，HUR/PIM1信号通路mRNA和蛋白含量升高，血管生成增加，Mdivi⁃1组效果相反。结论 Mdivi⁃1 降低线粒体的表达和 AngⅡ诱导的细胞的 HUR/PIM1 通路的表达，可抑制 AngⅡ诱导的细胞的凋亡、迁移及血管生成。

关键词:

线粒体, 高血压, HUR/PIM1, 血管内皮细胞

Abstract:

Objective To explore the mechanism of mitochondria in hypertensive vascular endothelial cell injury on based on the HUR/PIM1 signaling pathway. Methods HUVCE cells treated with different concentrations of AngⅡ were divided into three groups：a control group，AngⅡ group and Mdivi⁃1 group. Cell viability，apoptosis and migration rate were detected by CCK8，flow cytometry and Transwell. Mitochondrial ⁃ selective probes were used todetect mitochondrial morphology，and JC⁃1 dye was applied to measure mitochondrial membrane potential. Contents of intracellularDrp ⁃1，ROS，HUR/PIM1 mRNA and protein were detected by qPCR and Western blot， and angiogenesis was verified by angiogenesis in vitro. Results As compared with the control group，the AngⅡ group cell viability was decreased，expressions of Drp⁃1 and ROS proteins were increased，mitochondrial morphology was changed，membrane potential was declined，contents of mRNA and protein were enhanced in theHUR/PIM1 signaling pathway，and angiogenesis was increased. The effect of Mdivi ⁃1 group wason the contrary. Conclusions Mdivi⁃1 reduces mitochondria expression and expression of HUR/PIM1 pathway in AngⅡ⁃induced cells，and inhib⁃ its the apoptosis，migration and angiogenesis of AngⅡ⁃induced cells.

Key words:

mitochondria, hypertension, HUR/PIM1, vascular endothelial cells

尹磊蒋志明杨慧琼刘燕飞郑学斌 . 线粒体基于HUR/PIM1信号通路在高血压血管内皮细胞损伤中的机制 [J]. 实用医学杂志, 2022, 38(24): 3043-3048.

YIN Lei, JIANG Zhiming, YANG Huiqiong, LIU Yanfei, ZHENG Xuebin..

Mechanism of mitochondria⁃based HUR/PIM1 signaling pathway in hypertensive vascular endothelial cell injury [J]. The Journal of Practical Medicine, 2022, 38(24): 3043-3048.

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线粒体基于HUR/PIM1信号通路在高血压血管内皮细胞损伤中的机制

Mechanism of mitochondria⁃based HUR/PIM1 signaling pathway in hypertensive vascular endothelial cell injury

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