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iNOS及ERK1/2信号转导通路在17β-雌二醇抑制血管平滑肌细胞增殖中的作用

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第6期
页码:
761-764,773
栏目:
基础研究
出版日期:
2009-11-05

文章信息/Info

Title:
Effect of iNOS and ERK1/2 on 17β-estradiol-induced inhibition of vascular smooth muscle cell proliferation
作者:
刘海梅1赵晓峰2林桂平3徐进文3王庭槐3
1.广州中医药大学生理学教研室,广东 广州 510006;2.韶关学院医学院生理学教研室, 广东 韶关 512026;3.中山大学中山医学院生理学教研室,广东 广州 510080
Author(s):
LIU Hai-mei1 ZHAO Xiao-feng2 Lin Gui-ping3 XU Jin-wen3 WANG Ting-huai3
1.Department of Physiology, Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong, China; 2.Department of Physiology, Medical College of Shaoguan University, Shaoguan 512026, Guangdong, China; 3.Department of Physiology, Zhongshan Medical College, Sun-Yat Sen University, Guangzhou 510080, Guangdong, China
关键词:
17β-雌二醇诱导型一氧化氮合酶细胞外信号调节激酶1/2血管平滑肌细胞
Keywords:
17β-estradiol iNOS ERK1/2 vascular smooth muscle cell
分类号:
Q579.13
DOI:
-
文献标识码:
A
摘要:
目的: 观察诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)及细胞外信号调节激酶1/2(ERK1/2)信号转导通路在17β-雌二醇(17β-estradiol,E2)抑制血管平滑肌细胞(vascular smooth muscle cells,VSMCs)增殖中的作用。方法: 采用MTT比色法和Western blot技术,检测E2预处理前后胎牛血清(fetal calf serum,FCS)对VSMCs中DNA合成、iNOS表达及磷酸化的ERK1/2蛋白表达的影响。结果: E2作用24 h,可明显抑制FCS诱导的VSMCs增殖。Western blot的结果显示,FCS孵育VSMCs后,iNOS蛋白的表达下降,磷酸化的ERK1/2蛋白表达增加。E2预处理后,可增加iNOS蛋白的表达,抑制磷酸化ERK1/2蛋白表达。若提前应用iNOS阻断剂L-精氨酸甲酯(L-NAME)孵育VSMCs,可部分逆转E2诱导的磷酸化的ERK1/2蛋白表达下降的效应。结论: E2可抑制FCS诱导的VSMCs增殖,其作用可能与增加iNOS蛋白的表达,抑制磷酸化的ERK1/2表达有关。
Abstract:
AIM: To investigate the effect of iNOS and phosphorylation of ERK1/2 on 17β-estradiol (E2)-induced inhibition of vascular smooth muscle cells (VSMCs). METHODS: In cultured VSMCs, proliferation was determined by MTT assay, and the expression of iNOS and ERK1/2 phosphorylation were measured by Western blot. RESULTS: The measurement showed that exposure to fetal calf serum (FCS) for 24 h increased the proliferation of VSMCs. Pretreatment with E2 for 24 h inhibited VSMC proliferation under growth-stimulating (10% FCS) condition. Western blot showed that FCS inhibited expression of iNOS and increased expression of ERK1/2 phosphorylation in VSMCs. Pretreatment with E2 for 24 h partly reversed this effect. Western blot results further proved that pretreatment with iNOS inhibitor, L-NAME, partly reversed the increase of ERK1/2 phosphorylation induced by FCS. CONCLUSION: Our results demonstrate that 17β-estradiol increases iNOS expression and decreases ERK1/2 phosphorylation, leading to inhibition of VSMC proliferation.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期:2008-12-18.基金项目:国家自然科学基金项目资助(30440028) 通讯作者:王庭槐,教授,主要从事心血管疾病的实验研究及生物反馈研究Email:wangth@mail.sysu.edu.cn 作者简介:刘海梅,讲师,博士Email:happyliuhm@yahoo.com.cn
更新日期/Last Update: 2009-09-30