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作 者:尹磊[1] 蒋志明[1] 杨慧琼 刘燕飞[1] 郑学斌[1] YIN Lei;JIANG Zhiming;YANG Huiqiong;LIU Yanfei;ZHENG Xuebin(Department of Cardiology,the Fourth Hospital of Changsha,Changsha 410000,China)
出 处:《实用医学杂志》2022年第24期3043-3048,共6页The Journal of Practical Medicine
基 金:湖南省卫生健康委员会科研课题(编号:20200124)。
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。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 the HUR/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 inhibits the apoptosis,migration and angiogenesis of AngⅡ-induced cells.
分 类 号:R544.1[医药卫生—心血管疾病]
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