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|本期目录/Table of Contents|

血管紧张素II介导的大鼠血管平滑肌细胞STAT1激活与核转位(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2007年第1期
页码:
16-19
栏目:
基础研究
出版日期:
2007-01-01

文章信息/Info

Title:
Activation and nuclei translocation of STAT1 induced by Ang II in rat VSMCs
作者:
张海燕;  廖玉华; 魏宇淼; 孙艳香; 朱峰; 王敏; 郭和平
华中科技大学同济医学院心血管病研究所,附属协和医院心内科,湖北 武汉 430022
Author(s):
ZHANG Haiyan;  LIAO Yuhua;  WEI Yumiao;  SUN Yanxiang;  ZHU Feng;  WANG Min; GUO Heping
Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, Hubei, China
关键词:
血管平滑肌细胞; 血管紧张素II; 信号转导; 信号转导和转录活化因子
Keywords:
vascular smooth muscle cells;  Angiotensin II;  signal transduction pathways;  signal transducer and activators of transcription
分类号:
Q344
DOI:
-
文献标识码:
A
摘要:
目的 检测血管紧张素II(Ang II)介导的大鼠血管平滑肌细胞(VSMC)增殖过程中信号转导和转录活化因子1(STAT1)的激活与核转位。方法 本文采用Western印迹、非同位素凝胶电泳（EMSA）和免疫荧光染色的方法，观察Ang II刺激大鼠主动脉VSMC前后，细胞中STAT1的活化状态与定位。结果 VSMC经Ang II干预后, 胞内磷酸化的STAT1(pSTAT1)蛋白表达增加（P<0.01）,达峰后随时间梯度逐渐下降, Ang II干预15 min后检测到胞核内有蛋白DNA复合物形成。这一反应可被血管紧张素II 1型受体(AT1)阻滞剂Losartan以及Jak2抑制剂AG490抑制（P<0.01）。免疫荧光染色结果也显示Ang II干预后pSTAT1主要在胞核内表达。结论 Ang II可以通过和AT1受体结合,激活Jak/STAT通路,在Ang II介导的大鼠VSMC增殖过程中发挥作用。
Abstract:
AIM In vascular smooth muscle cells (VSMCs), the Janus kinase (Jak)/signal transducer and activators of transcription(STAT) is one of the induction of early growth response genes, and STAT proteins play an essential role in angiotensin IIinduced VSMC proliferation . To identify the activation and the nuclei translocation of signal transducers and activators of transcription1 (STAT1) induced by Ang II in the rat aortic smooth muscle cells. METHODS The cultured rat aortic smooth muscle cells were stimulated with Ang II. The protein expression of phosphorylation STAT1 was detected by Western blotting, STATSIE binding activation was detected by electrophoretic mobility shift assay and the nuclei translocation of phosphorylated STAT1 was identified by immunofluorescence. RESULTS Western blotting showed that the expression of phosphorylationSTAT1 in vascular smooth muscle cells (VSMCs) had an increase in Ang IIstimulated VSMCs（P<0.01）and the increase was blocked by Losartan（P<0.01）and AG490（P<0.01）. EMSA and immunofluorescence show that after a 15minute stimulation with Ang II, DNAprotein compounds were generated in the nucleus. This response could be blocked by Losartan. CONCLUSION JakSTAT signal transduction pathways participate and play a crucial role in the mechanism of Ang IIinduced VSMCs proliferation.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2006-02-23.基金项目：国家自然科学基金项目资助（No.G 30300133）通讯作者：廖玉华，教授，主任医师,主要从事心血管免疫学研究Emial:liaoyh27@hotmial.com 作者简介：张海燕，硕士生 Emial:apetrel@126.com
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