• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Perturbation by lysophosphatidylcholine of membrane permeability in cultured vascular smooth muscle and endothelial cells.
【24h】

Perturbation by lysophosphatidylcholine of membrane permeability in cultured vascular smooth muscle and endothelial cells.

机译：溶血磷脂酰胆碱对培养的血管平滑肌和内皮细胞的膜通透性的扰动。

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

Lysophosphatidylcholine (LPC), a major component of oxidized low-density lipoprotein found in atherosclerotic arterial walls, has been shown to have insignificant effect on arterial contraction but cause an impairment of endothelium-dependent relaxation (EDR). The aim of this study was to compare the degree of LPC-induced perturbation in the plasma membrane of cultured aortic smooth muscle cells (SMC) and endothelial cells (EC). In contractility studies phenylephrine (PE) elicited a sustained contraction and a subsequent addition of acetylcholine (ACh) caused an almost complete relaxation. Preincubation of endothelium-intact aortic rings with LPC did not significantly affect PE-elicited contraction but substantially inhibited ACh-triggered relaxation. Such inhibition by LPC was both concentration- and time-dependent. LPC also inhibited relaxation triggered by extracellular ATP and cyclopiazonic acid. Exposure of cultured EC to LPC (30 microM) resulted in an elevation of [Ca2+]i with a lag period of some 25 min. Following [Ca2+]i elevation, addition of Ni2+ resulted in a rapid entry of this ion into the cell. In addition, fura-2 leak-out was observed. Exposure of cultured SMC to 30 microM LPC also resulted in [Ca2+]i elevation and Ni2+ entry. However, LPC did not cause fura-2 leak-out in SMC. Also, LPC raised [Ca2+]i at a slower rate in SMC than in EC. Our results suggest that the plasma membrane of EC is more susceptible to LPC-induced derangement than that of SMC. This may contribute in part to the selective impairment of EDR by LPC.
机译：溶血磷脂酰胆碱（LPC）是动脉粥样硬化动脉壁中发现的氧化型低密度脂蛋白的主要成分，已显示对动脉收缩作用不明显，但会损害内皮依赖性舒张功能（EDR）。本研究的目的是比较LPC诱导的培养的主动脉平滑肌细胞（SMC）和内皮细胞（EC）质膜的扰动程度。在收缩性研究中，去氧肾上腺素（PE）引起持续收缩，随后添加乙酰胆碱（ACh）引起几乎完全松弛。用LPC对内皮完整的主动脉环进行预孵育不会显着影响PE引起的收缩，但会显着抑制ACh触发的松弛。 LPC的这种抑制作用与浓度和时间有关。 LPC还抑制细胞外ATP和环吡唑酸引发的松弛。培养的EC暴露于LPC（30 microM）导致[Ca2 +] i升高，滞后时间约为25分钟。在[Ca2 +] i升高后，添加Ni2 +导致该离子快速进入细胞。另外，观察到呋喃2泄漏。将培养的SMC暴露于30 microM LPC也会导致[Ca2 +] i升高和Ni2 +进入。但是，LPC不会在SMC中引起fura-2泄漏。而且，SMC中LPC升高[Ca2 +] i的速度比EC中慢。我们的结果表明，与SMC相比，EC的质膜更容易受到LPC诱导的脱位。这可能部分导致LPC对EDR的选择性损害。

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