...
首页> 外文期刊>Biophysical Chemistry: An International Journal Devoted to the Physical Chemistry of Biological Phenomena >A model of mitochondrial Ca(2+)-induced Ca2+ release simulating the Ca2+ oscillations and spikes generated by mitochondria.
【24h】

A model of mitochondrial Ca(2+)-induced Ca2+ release simulating the Ca2+ oscillations and spikes generated by mitochondria.

机译:线粒体Ca(2+)诱导的Ca2 +释放模型模拟了由线粒体产生的Ca2 +振荡和尖峰。

获取原文
获取原文并翻译 | 示例
           

摘要

Recent evidence underlines a key role of mitochondrial Ca2+ fluxes in cell Ca2+ signalling. We present here a kinetic model simulating the Ca2+ fluxes generated by mitochondria during mitochondrial Ca(2+)-induced Ca2+ release (mCICR) resulting from the operation of the permeability transition pore (PTP). Our model connects the Ca2+ fluxes through the ruthenium redsensitive Ca2+ uniporter, the respiration-dependent and passive H+ fluxes, the rate of oxygen consumption, the movements of weak acids across the mitochondrial membrane, the electrical transmembrane potential (delta psi), and operation of the PTP. We find that two factors are crucial to account for the various mCICR profiles that can be observed experimentally: (i) the dependence of PTP opening and closure on matrix pH (pHi), and (ii) the relative inhibition of the respiratory rate consecutive to PTP opening. The resulting model can simulate irreversible Ca2+ efflux from mitochondria, as well as the genesis of damped or sustained Ca2+ oscillations, and of single Ca2+ spikes. The model also simulates the main features of mCICR, i.e. the threshold-dependence of mCICR triggering, and the all-or-nothing nature of mCICR operation. Our model should appear useful to further mathematically address the consequences of mCICR on the spatiotemporal organisation of Ca2+ signals, as a 'plug-in' module for the existing models of cell Ca2+ signalling.
机译:最新证据强调线粒体Ca2 +通量在细胞Ca2 +信号传导中起关键作用。我们在这里提出了一个动力学模型,模拟了由线粒体Ca(2+)诱导的Ca2 +释放(mCICR)的线粒体在通透性过渡孔(PTP)操作中产生的Ca2 +通量。我们的模型将通过钌红色敏感Ca2 +单向通道的Ca2 +通量,依赖呼吸的H +通量和被动H +通量,耗氧率,弱酸在线粒体膜上的运动,跨膜电势(δpsi)和PTP。我们发现,两个因素对于解释可以通过实验观察到的各种mCICR曲线至关重要:(i)PTP打开和关闭对基质pH(pHi)的依赖性,以及(ii)连续呼吸速率对呼吸速率的相对抑制PTP开通。生成的模型可以模拟线粒体不可逆的Ca2 +流出,以及衰减或持续的Ca2 +振荡以及单个Ca2 +尖峰的发生。该模型还模拟了mCICR的主要特征,即mCICR触发的阈值依赖性以及mCICR操作的全有或全无。我们的模型应该看起来对进一步数学上解决mCICR对Ca2 +信号的时空组织的影响很有用,作为现有的细胞Ca2 +信号模型的“插入”模块。

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