AngⅡ对血管平滑肌细胞ANO1表达的影响及机制  

EFFECT OF ANGIOTENSIN II ON THE EXPRESSION OF ANOCTAMIN 1 IN VASCULAR SMOOTH MUSCLE CELLS AND RELATED MECHANISM

作　　者：迟晓琦 李浩然 吴雪[1] 张文秀 韩晓华[1] CHI Xiaoqi;LI Haoran;WU Xue;ZHANG Wenxiu;HAN Xiaohua(Department of Physiology and Pathophysiology,School of Basic Medicine,Qingdao University,Qingdao 266071,China)

机构地区：[1]青岛大学基础医学院生理学与病理生理学系,山东青岛266071

出　　处：《青岛大学学报（医学版）》2021年第2期214-217,共4页Journal of Qingdao University(Medical Sciences)

基　　金：山东省自然科学基金资助项目(ZR2019MH110);青岛市民生科技计划项目(19-6-1-19-nsh)。

摘　　要：目的探讨血管紧张素Ⅱ(AngⅡ)对大鼠血管平滑肌细胞(VSMCs)钙激活氯通道ANO1蛋白表达的影响及其受体机制。方法用不同浓度(1、10、100、500、1000 nmol/L)AngⅡ处理VSMCs 24 h或用100 nmol/L AngⅡ处理VSMCs不同时间(1、6、12、24、48 h),观察AngⅡ对ANO1表达的影响。AngⅡ处理(100 nmol/L,24 h)前分别加入血管紧张素Ⅰ型受体(AT1R)阻断剂氯沙坦钾(LP)和血管紧张素Ⅱ型受体(AT2R)阻断剂PD123319(PD),进一步探讨AngⅡ作用的受体机制。以组织贴块法进行大鼠VSMCs的原代培养,采用Western blot法检测ANO1蛋白表达水平。结果与对照组相比,以10~1000 nmol/L AngⅡ处理24 h可明显提高细胞中ANO1蛋白表达水平,其中以100 nmol/L AngⅡ的作用最为显著(F=18.56,P<0.01);与对照组相比较,以100 nmol/L AngⅡ处理12~48 h可显著上调细胞中ANO1蛋白的表达(F=10.84,P<0.01)。AT1R阻断剂LP可完全阻断AngⅡ诱导的ANO1表达(F=9.68,P<0.05),而AT2R阻断剂PD无此作用。结论AngⅡ以浓度和时间依赖性的方式显著上调VSMCs中ANO1蛋白的表达,该作用是通过AngⅡ与AT1R结合而实现的。Objective To investigate the effect of angiotensinⅡ(AngⅡ)on the expression of anoctamin 1(ANO1)in rat vascular smooth muscle cells(VSMCs)and its receptor mechanism.Methods VSMCs were treated with different concentrations of AngⅡ(1,10,100,500,and 1000 nmol/L)for 24 h or were treated with 100 nmol/L AngⅡfor different durations(1,6,12,24,and 48 h),and the effect of AngⅡon the expression of ANO1 was observed.The angiotensinⅡtype 1 receptor(AT1R)antagonist losartan potassium(LP)or the angiotensinⅡtype 2 receptor(AT2R)antagonist PD123319(PD)was added before the treatment with 100 nmol/L AngⅡfor 24 h to further explore the receptor mechanism of AngⅡ.The tissue patch me-thod was used for the primary culture of rat VSMCs,and Western blot was used to measure the protein expression level of ANO1.Results Compared with the control group,the cells treated with 10-1000 nmol/L AngⅡfor 24 h showed a significant increase in the protein expression level of ANO1,and 100 nmol/L AngⅡshowed the most significant effect(F=18.56,P<0.01).Compared with the control group,the cells treated with 100 nmol/L AngⅡfor 12-48 h had a significant increase in the protein expression of ANO1(F=10.84,P<0.01).The AT1R antagonist LP completely blocked the expression of ANO1 induced by AngⅡ(F=9.68,P<0.05),while the AT2R antagonist PD had no such effect.Conclusion AngⅡsignificantly upregulates the protein expression of ANO1 in VSMCs in a concentration-and time-dependent manner,possibly by binding to AT1R.

关 键 词：血管紧张素Ⅱ 肌细胞 平滑肌 氯化物通道 ANO1 受体 血管紧张素 大鼠 

分 类 号：R329.25[医药卫生—人体解剖和组织胚胎学] R544[医药卫生—基础医学]