...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cytokine >Effect of CCL5 on dimethylarginine dimethylaminohydrolase-1 production in vascular smooth muscle cells from spontaneously hypertensive rats
【24h】

Effect of CCL5 on dimethylarginine dimethylaminohydrolase-1 production in vascular smooth muscle cells from spontaneously hypertensive rats

机译：CCL5对自发性高血压大鼠血管平滑肌细胞中二甲基精氨酸二甲基氨基水解酶-1产生的影响

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Chemokines promote vascular inflammation and play a pathogenic role in the development and maintenance of hypertension. However, in our previous study, chemokine CCL5 was shown to reduce Ang II-induced 12-lipoxygenase (12-LO) production as well as proliferation in vascular smooth muscle cells (VSMCs) obtained from spontaneously hypertensive rats (SHR). Dimethylarginine dimethylaminohydrolase (DDAH) acts as an important regulator of vascular function by metabolizing and regulating plasma asymmetric (NG,NG) dimethylarginine (ADMA), a major risk factor for cardiovascular disease. Therefore, in this study, we investigated the effect of CCL5 on DDAH-1 production in SHR VSMCs. Constitutive expression of DDAH-1 in VSMCs from SHR was higher than that in VSMCs from normotensive Wistar Kyoto rats (WKY), whereas expression of DDAH-2 was not significantly different between SHR and WKY VSMCs. CCL5 increased DDAH-1 production and attenuated Ang II-induced DDAH-1 inhibition in SHR VSMCs. In addition, although CCL5 did not affect the level of asymmetric (NG,NG) dimethylarginine (ADMA), it attenuated Ang II-induced ADMA production through DDAH-1 activity. DDAH-1 induction by CCL5 was mediated by the Ang II subtype 2 receptor (AT2 R) pathway. Further, attenuation of Ang II-induced 12-LO and endothelin-1 (ET-1) expression by CCL5 could be attributed to DDAH-1 activity. These findings combined with our previous results suggest that CCL5 is a potential down-regulatory factor in Ang II-induced vascular hypertension.
机译：趋化因子促进血管炎症，并在高血压的发生和维持中起致病作用。然而，在我们先前的研究中，趋化因子CCL5可以减少Ang II诱导的12-脂氧合酶（12-LO）的产生以及自发性高血压大鼠（SHR）获得的血管平滑肌细胞（VSMC）的增殖。二甲基精氨酸二甲基氨基水解酶（DDAH）通过代谢和调节血浆不对称（NG，NG）二甲基精氨酸（ADMA）（一种心血管疾病的主要危险因素），起着重要的血管功能调节剂的作用。因此，在这项研究中，我们调查了CCL5对SHR VSMC中DDAH-1产生的影响。 SHR的VSMC中DDAH-1的组成型表达高于正常血压Wistar Kyoto大鼠（WKY）的VSMC，而DDAH-2的表达在SHR和WKY VSMC中没有显着差异。 CCL5增加了SHR VSMC中DDAH-1的产生并减弱了Ang II诱导的DDAH-1抑制。此外，尽管CCL5不会影响不对称（NG，NG）二甲基精氨酸（ADMA）的水平，但它通过DDAH-1活性减弱了Ang II诱导的ADMA产生。 CCL5诱导DDAH-1由Ang II亚型2受体（AT2 R）途径介导。此外，CCL5对Ang II诱导的12-LO和内皮素1（ET-1）表达的减弱可能归因于DDAH-1活性。这些发现与我们以前的结果相结合，表明CCL5是Ang II诱导的血管高血压的潜在下调因子。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号