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Structural and Mechanical Changes in Heart Mitochondria of Rat by AFM

机译:AFM鼠心肌线粒体的结构和机械变化

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Mitochondria play critical roles in both the life and death of cardiac myocytes. Various factors such as loss of ATP synthesis and increase of ATP hydrolysis, impairment in ionic homeostasis, formation of reactive oxygen species (ROS) and release of proapoptotic proteins are related to the generation of irreversible damage. It has been proposed that the release of cytochrome c is caused by a swelling of the mitochondrial matrix triggered by the apoptotic stimuli. But there is a controversy about whether or not the mitochondria indeed swell -during apoptosis. In this study, we observed the morphological and property changes in heart mitochondria which were isolated from rat myocardial infarction model using AFM. The normal mitochondria showed a homogeneous distribution with similar sizes and shapes. The surfaces of normal mitochondria looked smooth and had integrity. However, irregularities in the shapes and sizes of mitochondria were observed in those of ischemic rats. And the surfaces of ischemic mitochondria became rugged. Ultrastructural analysis of mitochondria utilizing AFM demonstrated that myocardial infarction resulted in significant increase in heart mitochondrial size, as compared with that of normal mitochondria. The force-distance curve measurements were performed to investigate the change in the adhesive force of mitochondria affected by myocardial infarction. We inferred that the changes in the adhesion force of mitochondria might be related to destruction of the highly dense mitochondrial outer membrane by swelling.
机译:线粒体在心肌细胞的生命和死亡中发挥着关键作用。各种因素,如ATP合成损失和ATP水解的增加,离子稳态的损伤,反应性氧物质(ROS)的形成和促凋亡蛋白的释放与不可逆损伤的产生有关。已经提出,细胞色素C的释放是由凋亡刺激触发的线粒体基质的肿胀引起的。但是,线粒体是否确实肿胀的细胞凋亡存在争议。在这项研究中,我们观察到使用AFM从大鼠心肌梗死模型中分离的心脏线粒体的形态和性质变化。正常线粒体显示出具有相似尺寸和形状的均匀分布。正常线粒体的表面看起来光滑,诚信。然而,在缺血性大鼠的那些中观察到线粒体的形状和尺寸的不规则性。缺血性线粒体的表面变得崎岖。利用AFM的线粒体超微结构分析表明,与正常线粒体相比,心肌梗塞的心肌梗死率显着增加。进行力 - 距离测量以研究受心肌梗死影响的线粒体粘附力的变化。我们推断线粒体粘附力的变化可能与溶胀的高致密线粒体外膜的破坏有关。

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