• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>Antioxidants >Oxidative Stress Increases Endogenous Complement-Dependent Inflammatory and Angiogenic Responses in Retinal Pigment Epithelial Cells Independently of Exogenous Complement Sources
【2h】

Oxidative Stress Increases Endogenous Complement-Dependent Inflammatory and Angiogenic Responses in Retinal Pigment Epithelial Cells Independently of Exogenous Complement Sources

机译：氧化应激增加视网膜色素上皮细胞的内源性补体依赖性炎性和血管生成反应独立于外源性补体来源

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Oxidative stress-induced damage of the retinal pigment epithelium (RPE) and chronic inflammation have been suggested as major contributors to a range of retinal diseases. Here, we examined the effects of oxidative stress on endogenous complement components and proinflammatory and angiogenic responses in RPE cells. ARPE-19 cells exposed for 1–48 h to H O had reduced cell–cell contact and increased markers for epithelial–mesenchymal transition but showed insignificant cell death. Stressed ARPE-19 cells increased the expression of complement receptors CR3 (subunit CD11b) and C5aR1. CD11b was colocalized with cell-derived complement protein C3, which was present in its activated form in ARPE-19 cells. C3, as well as its regulators complement factor H (CFH) and properdin, accumulated in the ARPE-19 cells after oxidative stress independently of external complement sources. This cell-associated complement accumulation was accompanied by increased and expression and the subsequently enhanced secretion of proinflammatory and proangiogenic factors. The complement-associated ARPE-19 reaction to oxidative stress, which was independent of exogenous complement sources, was further augmented by the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib. Our results indicate that ARPE-19 cell-derived complement proteins and receptors are involved in ARPE-19 cell homeostasis following oxidative stress and should be considered as targets for treatment development for retinal degeneration.
机译：氧化应激诱导的视网膜色素上皮（RPE）损伤和慢性炎症已被认为是造成一系列视网膜疾病的主要因素。在这里，我们检查了氧化应激对RPE细胞内源性补体成分以及促炎和血管生成反应的影响。暴露于H O 1–48 h的ARPE-19细胞减少了细胞间接触，增加了上皮-间质转化的标记物，但显示出微不足道的细胞死亡。紧张的ARPE-19细胞增加补体受体CR3（亚基CD11b）和C5aR1的表达。 CD11b与细胞衍生的补体蛋白C3共定位，后者以活化形式存在于ARPE-19细胞中。 C3及其调节因子补体因子H（CFH）和备解素在氧化应激后积累在ARPE-19细胞中，与外部补体来源无关。这种与细胞相关的补体积累伴随着促炎和促血管生成因子的表达增加以及随后的分泌增加。聚（ADP-核糖）聚合酶（PARP）抑制剂olaparib进一步增强了与氧化应激相关的与补体相关的ARPE-19反应，该反应独立于外源补体来源。我们的结果表明，ARPE-19细胞衍生的补体蛋白和受体参与氧化应激后的ARPE-19细胞稳态，应被认为是视网膜变性治疗发展的目标。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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