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Mitochondrial transplantation enhances murine lung viability and recovery after ischemia-reperfusion injury.

线粒体移植增强小鼠肺活力和缺血再灌注损伤后的恢复。

  • 影响因子:3.82
  • DOI:10.1152/ajplung.00221.2019
  • 作者列表:"Moskowitzova K","Orfany A","Liu K","Ramirez-Barbieri G","Thedsanamoorthy JK","Yao R","Guariento A","Doulamis IP","Blitzer D","Shin B","Snay ER","Inkster JAH","Iken K","Packard AB","Cowan DB","Visner GA","Del Nido PJ","McCully JD
  • 发表时间:2020-01-01
Abstract

:The most common cause of acute lung injury is ischemia-reperfusion injury (IRI), during which mitochondrial damage occurs. We have previously demonstrated that mitochondrial transplantation is an efficacious therapy to replace or augment mitochondria damaged by IRI, allowing for enhanced muscle viability and function in cardiac tissue. Here, we investigate the efficacy of mitochondrial transplantation in a murine lung IRI model using male C57BL/6J mice. Transient ischemia was induced by applying a microvascular clamp on the left hilum for 2 h. Upon reperfusion mice received either vehicle or vehicle-containing mitochondria either by vascular delivery (Mito V) through the pulmonary artery or by aerosol delivery (Mito Neb) via the trachea (nebulization). Sham control mice underwent thoracotomy without hilar clamping and were ventilated for 2 h before returning to the cage. After 24 h recovery, lung mechanics were assessed and lungs were collected for analysis. Our results demonstrated that at 24 h of reperfusion, dynamic compliance and inspiratory capacity were significantly increased and resistance, tissue damping, elastance, and peak inspiratory pressure (Mito V only) were significantly decreased (P < 0.05) in Mito groups as compared with their respective vehicle groups. Neutrophil infiltration, interstitial edema, and apoptosis were significantly decreased (P < 0.05) in Mito groups as compared with vehicles. No significant differences in cytokines and chemokines between groups were shown. All lung mechanics results in Mito groups except peak inspiratory pressure in Mito Neb showed no significant differences (P > 0.05) as compared with Sham. These results conclude that mitochondrial transplantation by vascular delivery or nebulization improves lung mechanics and decreases lung tissue injury.

摘要

急性肺损伤最常见的原因是缺血再灌注损伤 (IRI),在此期间线粒体损伤发生。我们之前已经证明,线粒体移植是替代或增加 IRI 损伤的线粒体的有效疗法,允许增强心脏组织中的肌肉活力和功能。在此,我们使用雄性 C57BL/6J 小鼠在小鼠肺 IRI 模型中研究线粒体移植的疗效。用微血管钳夹左侧肺门 2 h 诱导短暂性缺血。再灌注后,小鼠通过血管递送 (Mito V) 通过肺动脉或气溶胶递送 (Mito Neb) 通过气管 (雾化) 接受溶剂或含溶剂的线粒体。假对照小鼠开胸不夹闭肺门,通气 2 h 后再回笼。恢复 24 h 后,评估肺力学并收集肺进行分析。我们的结果表明,在再灌注 24 h 时,动态顺应性和吸气容量显著增加,阻力、组织阻尼、弹性和吸气峰压 (仅 Mito V) 与各自的溶剂组相比,Mito 组显著降低 (P 0.05)。这些结果表明,通过血管递送或雾化吸入的线粒体移植改善了肺力学并减少了肺组织损伤。

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影响因子:3.94
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DOI:10.1016/j.taap.2019.114847
作者列表:["Bernstein DM","Toth B","Rogers RA","Kling DE","Kunzendorf P","Phillips JI","Ernst H"]

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关键词: 暂无
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影响因子:4.04
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DOI:10.1042/BST20191010
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