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血管紧张素Ⅱ通过核因子κB上调巨噬细胞基质金属蛋白酶诱导因子的表达 被引量：3

Angiotensin Ⅱ Induces Extracellular Matrix Metalloproteinase Inducer Expression in THP-1 Macrophages via a Nuclear Factor-κB Pathway
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摘要 目的观察血管紧张素Ⅱ对巨噬细胞表达基质金属蛋白酶诱导因子的影响及其相关通路。方法血管紧张素Ⅱ体外刺激人巨噬细胞,应用逆转录聚合酶链反应和Western blot测定基质金属蛋白酶诱导因子基因和蛋白表达;RNA干扰技术沉默核转录因子核因子κB p65亚基,评价核因子κB通路在血管紧张素Ⅱ上调巨噬细胞细胞基质金属蛋白酶诱导因子的表达中的作用。结果血管紧张素Ⅱ刺激巨噬细胞后,基质金属蛋白酶诱导因子mRNA和蛋白表达均显著增加,核因子κB p65亚基沉默后,血管紧张素Ⅱ对基质金属蛋白酶诱导因子mRNA和蛋白表达无上调作用。结论血管紧张素Ⅱ上调基质金属蛋白酶诱导因子的表达,此调控过程有核因子κB通路的参与。 Aim To evaluate the effect of AngiotensinⅡon EMMPRIN expression in THP-1 macrophage and its potential mechanism. Methods Macrophages cell line was esteblished by induced THP-1 using PMA,and then the effect of AngⅡ on EMMPRIN expression on THP-1 macrophages was investigated. Results RT-PCR and Western Blot showed that AngⅡ upregulated EMMPRIN expression in a dose and time dependent manner.Either nuclear factor-κB inhibitor PDTC or P65 RNAi treatment can suppress the effect of angⅡon EMMPRIN. Conclusion AngⅡupregulates the expression of EMMPRIN.Nuclear factor-κB is the critical factor involving in the EMMPRIN upregulation induced by angⅡ.
作者 刘宏 杨丽霞 郭瑞威 叶金善 齐峰 王先梅 郭传明 梁星
机构地区 成都军区昆明总医院心血管内科
出处 《中国动脉硬化杂志》 CAS CSCD 北大核心 2009年第8期669-673,共5页 Chinese Journal of Arteriosclerosis
关键词 血管紧张素Ⅱ 细胞基质金属蛋白酶诱导因子 核因子ΚB THP-1巨噬细胞 Angiotensin II Extracellular Matrix Metalloproteinase Inducer Nuclear Factor-κB THP-1 macrophages
分类号 R5 [医药卫生—内科学]
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参考文献22

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同被引文献19

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中国动脉硬化杂志
2009年 第8期

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