Effects of hypoxia-reoxygenation stress on mitochondrial proteome and bioenergetics of the hypoxia-tolerant marine bivalve Crassostrea gigas.
Effects of hypoxia-reoxygenation stress on mitochondrial proteome and bioenergetics of the hypoxia-tolerant marine bivalve Crassostrea gigas.
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缺氧-复氧应激对耐缺氧海洋双壳类巨牡蛎线粒体蛋白质组和生物能的影响
DOI：
10.1016/j.jprot.2018.12.009
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发表时间：
2019
影响因子：
3.3
通讯作者：
Sokolova
中科院分区：
文献类型：
--
作者：
Sokolov;Markert;Hinzke;Hirschfeld;Becher;Ponsuksili;Sokolova
线粒体是缺氧-复氧（H/R）应激的关键细胞内靶点，因为它们在ATP和活性氧（ROS）的产生中起中心作用。潮间带牡蛎Crassostrea gigasare适应频繁的H/R周期，并保持有氧功能，尽管频繁的氧气波动。为了深入了解H/R耐受的分子机制，我们评估了线粒体呼吸和（磷酸）蛋白质组的变化。在缺氧和恢复期间产生了10亿次的气体。牡蛎线粒体保持OXPHOS能力，尽管细胞色素氧化酶活性下降，在H/R胁迫。在H/R应激过程中线粒体蛋白质组的重排涉及线粒体电子传递系统和铁结合蛋白的上调，以及将电子传递到泛醌的途径的抑制，可能作为限制ROS产生的机制。H/R应激导致了一种线粒体吞噬激活剂PGAM 5的上调和金属内肽酶OMA 1的去磷酸化，表明线粒体质量控制机制的刺激。参与线粒体蛋白质稳态的关键蛋白质的丰度和磷酸化水平的变化表明缺氧期间蛋白质合成的抑制，可能是一种节能机制，以及其随后在复氧期间的重新激活。因此，线粒体的变化缺氧-复氧（H/R）胁迫引起牡蛎线粒体蛋白质组和磷酸化蛋白质组的变化，上调电子传递系统的表达，促进线粒体的功能，从而提高牡蛎的耐缺氧能力。限制电子流向泛醌并激活线粒体质量控制和蛋白质稳态机制。这些研究结果提供了深入了解蛋白质组学变化在适应性反应H/R应激中的潜在作用，并作为理解线粒体对缺氧和复氧敏感性机制的重要基准。
Mitochondria are key intracellular targets of hypoxia-reoxygenation (H/R) stress due to their central role in generation of ATP and reactive oxygen species (ROS). Intertidal oystersCrassostrea gigasare adapted to frequent H/R cycles and maintain aerobic function despite frequent oxygen fluctuations. To gain insight into the molecular mechanisms of H/R tolerance, we assessed changes in mitochondrial respiration and (phospho)proteome ofC. gigasduring hypoxia and recovery. Oyster mitochondria maintained OXPHOS capacity despite a decline in cytochromecoxidase activity during H/R stress. Rearrangements of the mitochondrial proteome during H/R stress involved upregulation of mitochondrial electron transport system and iron-binding proteins, and suppression of the pathways that channel electrons to ubiquinone, possibly as a mechanism to limit ROS production. H/R stress led to upregulation of a mitophagic activator PGAM5 and dephosphorylation of metalloendopeptidase OMA1, indicating stimulation of mitochondrial quality control mechanisms. Changes in abundance and phosphorylation levels of key proteins involved in mitochondrial protein homeostasis indicate suppression of protein synthesis during hypoxia, likely as an energy-saving mechanism, and its subsequent reactivation during reoxygenation. Thus, shifts in the mitochondrial (phospho-)proteome might play an important role in H/R stress resistance of oysters ensuring mitochondrial integrity and function during oxygen fluctuations.SignificanceHypoxia-reoxygenation (H/R) stress elicits shifts in proteome and phosphoproteome of mitochondria in a hypoxia-tolerant model bivalve, oysterCrassostrea gigas, upregulating electron transport system, limiting electron flow to ubiquinone and activating mitochondrial quality control and protein homeostasis mechanisms. These findings provide insights into the potential role of proteomic shifts in adaptive response to H/R stress and serve as an important benchmark to understand the mechanisms of mitochondrial sensitivity to hypoxia and reoxygenation.
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DOI：
10.1016/b978-0-12-394309-5.00006-7
发表时间：
2012
影响因子：
--
作者：
Kalogeris, Theodore;Baines, Christopher P.;Krenz, Maike;Korthuis, Ronald J.
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DOI：
10.1016/j.cbpb.2016.08.004
发表时间：
2016
期刊：
Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology
影响因子：
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作者：
S. Green;K. Storey
通讯作者：
K. Storey
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2006-10
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The Chinese journal of physiology
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DOI：
10.1152/ajpheart.00708.2002
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2003-02-01
影响因子：
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DOI：
--
发表时间：
1991
期刊：
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