• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Interaction of myeloperoxidase with vascular NAD(P)H oxidase-derived reactive oxygen species in vasculature: implications for vascular diseases.
【24h】

Interaction of myeloperoxidase with vascular NAD(P)H oxidase-derived reactive oxygen species in vasculature: implications for vascular diseases.

机译：髓过氧化物酶与血管中NAD（P）H氧化酶衍生的活性氧的相互作用：对血管疾病的影响。

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

Vascular NAD(P)H oxidase-derived reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) have emerged as important molecules in the pathogenesis of atherosclerosis, hypertension, and diabetic vascular complications. Additionally, myeloperoxidase (MPO), a transcytosable heme protein that is derived from leukocytes, is also believed to play important roles in the above-mentioned inflammatory vascular diseases. Previous studies have shown that MPO-induced vascular injury responses are H2O2 dependent. It is well known that MPO can use leukocyte-derived H2O2; however, it is unknown whether the vascular-bound MPO can use vascular nonleukocyte oxidase-derived H2O2 to induce vascular injury. In the present study, ANG II was used to stimulate vascular NAD(P)H oxidases and increase their H2O2 production in the vascular wall, and vascular dysfunction was used as the vascular injury parameter. We demonstrated that vascular-bound MPO has sustained activity in the vasculature. MPO could use the vascular NAD(P)H oxidase-derived H2O2 to produce hypochlorus acid (HOCl) and its chlorinating species. More importantly, MPO derived HOCl and chlorinating species amplified the H2O2-induced vascular injury by additional impairment of endothelium-dependent relaxation. HOCl-modified low-density lipoprotein protein (LDL), a specific biomarker for the MPO-HOCl-chlorinating species pathway, was expressed in LDL and MPO-bound vessels with vascular NAD(P)H oxidase-derived H2O2. MPO-vascular NAD(P)H oxidase-HOCl-chlorinating species may represent a common pathogenic pathway in vascular diseases and a new mechanism involved in exacerbation of vascular diseases under inflammatory conditions.
机译：血管NAD（P）H氧化酶衍生的活性氧（ROS），例如过氧化氢（H2O2）已成为动脉粥样硬化，高血压和糖尿病性血管并发症的重要分子。另外，还认为髓过氧化物酶（MPO）是一种源自白细胞的可转细胞血红素蛋白，在上述炎症性血管疾病中也起着重要作用。先前的研究表明，MPO诱导的血管损伤反应是H2O2依赖性的。众所周知，MPO可以使用白细胞衍生的H2O2。但是，与血管结合的MPO是否可以使用源自血管非白细胞氧化酶的H2O2引起血管损伤尚不清楚。在本研究中，ANG II被用于刺激血管NAD（P）H氧化酶并增加其在血管壁中的H2O2产生，而血管功能障碍则被用作血管损伤参数。我们证明了血管结合的MPO在脉管系统中具有持续的活性。 MPO可以使用血管NAD（P）H氧化酶衍生的H2O2生成次氯酸（HOCl）及其氯化物。更重要的是，MPO衍生的HOCl和氯化物会进一步损害内皮依赖性舒张功能，从而加剧H2O2诱导的血管损伤。 HOCl修饰的低密度脂蛋白蛋白（LDL）是MPO-HOCl氯化物种途径的特定生物标记，在带有血管NAD（P）H氧化酶的H2O2的LDL和MPO结合血管中表达。 MPO-血管NAD（P）H氧化酶-HOCl氯化物种可能代表血管疾病中的常见致病途径，并且是炎症条件下加剧血管疾病的新机制。

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