• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Ca2+ uptake in mitochondria occurs via the reverse action of the Na+/Ca2+ exchanger in metabolically inhibited MDCK cells.
【24h】

Ca2+ uptake in mitochondria occurs via the reverse action of the Na+/Ca2+ exchanger in metabolically inhibited MDCK cells.

机译：线粒体中的Ca2 +吸收是通过Na + / Ca2 +交换子在代谢抑制的MDCK细胞中的逆作用而发生的。

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

In ischemic or hypoxic tissues, elevated Ca2+ levels have emerged as one of the main damaging agents among other Ca2+-independent mechanisms of cellular injury. Because mitochondria, besides the endoplasmic reticulum, play a key role in the maintainance of cellular Ca2+ homeostasis, alterations in the mitochondrial Ca2+ content ([Ca2+]m) were monitored in addition to changes in cytosolic Ca2+ concentration ([Ca2+]i) during metabolic inhibition (MI) in renal epithelial Madin-Darby canine kidney (MDCK) cells. [Ca2+]i and [Ca2+]m were monitored via, respectively, fura 2 and rhod 2 measurements. MI induced an increase in [Ca2+]i reaching 631+/-78 nM in approximately 20 min, followed by a decrease to 118+/-9 nM in the next approximately 25 min. A pronounced drop in cellular ATP levels and a rapid increase in intracellular Na+ concentrations in the first 20 min of MI excluded Ca2+ efflux in the second phase via plasma membrane ATPases or Na+/Ca2+ exchangers (NCE). Mitochondrial rhod 2 intensities increased to 434+/-46% of the control value during MI, indicating that mitochondria sequester Ca2+ during MI. The mitochondrial potential (deltapsim) was lost in 20 min of MI, excluding mitochondrial Ca2+ uptake via the deltapsim-dependent mitochondrial Ca2+ uniporter after 20 min of MI. Under Na+-free conditions, or when CGP-37157, a specific inhibitor of the mitochondrial NCE, was used, no drop in [Ca2+]i was seen during MI, whereas the MI-induced increase in mitochondrial rhod 2 fluorescence was strongly reduced. To our knowledge, this study is the first to report that in metabolically inhibited renal epithelial cells mitochondria take up Ca2+ via the NCE acting in the reverse mode.
机译：在局部缺血或缺氧的组织中，升高的Ca2 +水平已成为细胞损伤的其他与Ca2 +无关的机制中的主要破坏因素之一。由于线粒体除内质网外，在维持细胞内Ca2 +稳态中也起着关键作用，因此除了代谢过程中细胞质中Ca2 +浓度（[Ca2 +] i）的变化外，还监测了线粒体Ca2 +含量（[Ca2 +] m）的变化。肾上皮Madin-Darby犬肾（MDCK）细胞中的抑制（MI）。 [Ca2 +] i和[Ca2 +] m分别通过呋喃2和Rhod 2测量进行监测。 MI引起[Ca2 +] i的增加，在大约20分钟内达到631 +/- 78 nM，然后在接下来的大约25分钟内降低到118 +/- 9 nM。在MI的前20分钟内，细胞ATP水平的明显下降和细胞内Na +浓度的快速增加排除了第二阶段通过质膜ATPase或Na + / Ca2 +交换剂（NCE）引起的Ca2 +外流。心肌梗死期间线粒体rho 2强度增加至对照值的434 +/- 46％，表明心肌梗死期间线粒体螯合Ca2 +。 MI后20分钟，线粒体电位（deltapsim）消失，MI后20分钟后，线粒体Ca2 +的摄取通过deltapsim依赖的线粒体Ca2 +单向转运体而消失。在无Na +的条件下，或当使用线粒体NCE的特异性抑制剂CGP-37157时，MI期间[Ca2 +] i没有下降，而MI诱导的线粒体Rhod 2荧光的增加却大大降低了。据我们所知，该研究是第一个报道在代谢抑制的肾上皮细胞中线粒体通过逆向作用的NCE吸收Ca2 +的研究。

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