Oxidative stress disrupts oligodendrocyte maturation.
Oxidative stress disrupts oligodendrocyte maturation.
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DOI：
10.1002/jnr.22139
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发表时间：
2009-11-01
影响因子：
4.2
通讯作者：
Grinspan, Judith B.
中科院分区：
文献类型：
--
作者：
French, Heather Morein;Reid, Mary;Mamontov, Polina;Simmons, Rebecca A.;Grinspan, Judith B.
脑室周围白质损伤(PWMI)是早产幸存者慢性神经损伤的主要原因。PWMI的特点是髓鞘过少，缺乏成熟的髓鞘少突胶质细胞。少突胶质细胞经历了从神经干细胞到成熟少突胶质细胞的谱系演变过程。与成熟的少突胶质细胞相比，少突胶质细胞前体细胞对氧化和自由基介导的损伤的敏感性增加，这是因为抗氧化酶和自由基清除剂的水平较低。在这项研究中，我们发现氧化应激通过两种机制破坏少突胶质细胞的分化。首先，氧化剂减少了神经干细胞中促进少突胶质细胞分化的关键基因的表达，增加了已知的抑制分化的基因的表达。第二，全局性组蛋白乙酰化在氧化应激条件下持续存在，进一步有助于防止少突胶质细胞分化。这两种机制都可以阻止少突胶质细胞的分化，而不会增加细胞死亡。
Periventricular white matter injury (PWMI), is the leading cause of chronic neurologic injury among survivors of preterm birth. The hallmark of PWMI is hypomyelination and a lack of mature, myelinating oligodendrocytes. Oligodendrocytes undergo a well-characterized lineage progression from neural stem cell to mature oligodendrocyte. Oligodendrocyte precursors have increased susceptibility to oxidative and free radical-mediated injury compared to mature oligodendrocytes due to lower levels of anti-oxidant enzymes and free radical scavengers. In this study, we show that oxidative stress disrupts oligodendrocyte differentiation by two mechanisms. First, oxidizing agents decrease the expression of key genes which promote oligodendrocyte differentiation from neural stem cells and increase the expression of genes known to inhibit differentiation. Second, global histone acetylation persists under conditions of oxidative stress, further contributing to the prevention of oligodendrocyte differentiation. Both of these mechanisms result in the arrest of oligodendrocyte differentiation without an increase in cell death.
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影响因子：
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作者：
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