Changes to mitochondrial ultrastructure in optic nerve vulnerable to secondary degeneration in vivo are limited by irradiation at 670 nm.
Changes to mitochondrial ultrastructure in optic nerve vulnerable to secondary degeneration in vivo are limited by irradiation at 670 nm.
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DOI：
10.1186/1471-2202-14-98
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发表时间：
2013-09-08
期刊：
影响因子：
2.4
通讯作者：
Fitzgerald M
中科院分区：
文献类型：
--
作者：
Cummins N;Bartlett CA;Archer M;Bartlett E;Hemmi JM;Harvey AR;Dunlop SA;Fitzgerald M
中枢神经系统的创伤性损伤会导致原发性损伤以外的组织损伤，称为继发性变性。被认为与继发性变性相关的关键事件涉及线粒体功能的各个方面，这些功能可能受到红光/近红外辐射疗法（R/NIR-IT）的调节，但线粒体在体内如何受到影响尚未得到研究。通过横切成年大鼠视神经的背侧来模拟继发性变性，并通过透射电子显微镜研究易受继发性变性影响的完整腹侧视神经的线粒体超微结构。尽管有报道称中枢神经系统损伤后裂变增加，但我们发现体内易发生继发性变性的视神经线粒体密度没有变化。然而，在轴突中，线粒体轮廓区域的频率分布显示损伤后第一天较小线粒体轮廓的累积概率较高。神经胶质线粒体轮廓没有表现出面积变化，但在损伤后第 1 天和第 7 天观察到更椭圆的线粒体形状。重要的是，在体内易发生继发性变性的视神经中，在第1天和第7天观察到线粒体自噬特征。柠檬酸合酶活性被用作腹侧视神经线粒体质量的额外测量，并在第 7 天下降，而线粒体顺乌头酸酶活性在易发生继发性变性的视神经损伤后第 1 天和第 28 天增加。 R/NIR-IT 已用于治疗受损的中枢神经系统，据报道氧化代谢有所改善，表明线粒体参与，但缺乏超微结构信息。在这里，我们表明，受伤动物的 R/NIR-IT 导致线粒体区域和形状的分布与对照没有显着差异，并且线粒体自噬特征显着降低。 R/NIR-IT 还导致易发生继发性变性的视神经柠檬酸合酶活性降低（第 7 天）和乌头酸酶活性增加（第 1 天）。这些发现表明，线粒体结构和柠檬酸循环酶的活性在体内二次变性过程中发生动态改变，R/NIR-IT 可以保护线粒体结构。
Traumatic injury to the central nervous system results in damage to tissue beyond the primary injury, termed secondary degeneration. Key events thought to be associated with secondary degeneration involve aspects of mitochondrial function which may be modulated by red/near-infrared irradiation therapy (R/NIR-IT), but precisely how mitochondria are affected in vivo has not been investigated. Secondary degeneration was modelled by transecting the dorsal aspect of the optic nerve in adult rats and mitochondrial ultrastructure in intact ventral optic nerve vulnerable to secondary degeneration investigated with transmission electron microscopy. Despite reported increases in fission following central nervous system injury, we saw no change in mitochondrial densities in optic nerve vulnerable to secondary degeneration in vivo. However, in axons, frequency distributions of mitochondrial profile areas showed higher cumulative probabilities of smaller mitochondrial profiles at day 1 after injury. Glial mitochondrial profiles did not exhibit changes in area, but a more elliptical mitochondrial shape was observed at both day 1 and 7 following injury. Importantly, mitochondrial autophagic profiles were observed at days 1 and 7 in optic nerve vulnerable to secondary degeneration in vivo. Citrate synthase activity was used as an additional measure of mitochondrial mass in ventral optic nerve and was decreased at day 7, whereas mitochondrial aconitase activity increased at day 1 and day 28 after injury in optic nerve vulnerable to secondary degeneration. R/NIR-IT has been used to treat the injured central nervous system, with reported improvements in oxidative metabolism suggesting mitochondrial involvement, but ultrastructural information is lacking. Here we show that R/NIR-IT of injured animals resulted in distributions of mitochondrial areas and shape not significantly different from control and significantly reduced mitochondrial autophagic profiles. R/NIR-IT also resulted in decreased citrate synthase activity (day 7) and increased aconitase activity (day 1) in optic nerve vulnerable to secondary degeneration. These findings suggest that mitochondrial structure and activity of enzymes of the citric acid cycle are dynamically altered during secondary degeneration in vivo and R/NIR-IT may protect mitochondrial structure.
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9.2
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