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首页> 外文期刊>The European Journal of Neuroscience >Maintenance of the relative proportion of oligodendrocytes to axons even in the absence of BAX and BAK.
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Maintenance of the relative proportion of oligodendrocytes to axons even in the absence of BAX and BAK.

机译：即使在没有BAX和BAK的情况下，也能维持少突胶质细胞与轴突的相对比例。

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Highly purified oligodendroglial lineage cells from mice lacking functional bax and bak genes were resistant to apoptosis after in-vitro differentiation, indicating an essential role of the intrinsic apoptotic pathway in apoptosis of oligodendrocytes in the absence of neurons (axons) and other glial cells. These mice therefore provide a valuable tool with which to evaluate the significance of the intrinsic apoptotic pathway in regulating the population sizes of oligodendrocytes and oligodendroglial progenitor cells. Quantitative analysis of the optic nerves and the dorsal columns of the spinal cord revealed that the absolute numbers of mature oligodendrocytes immunolabeled for aspartoacylase and adult glial progenitor cells expressing NG2 chondroitin sulfate proteoglycan were increased in both white matter tracts of adult bax/bak-deficient mice and, to a lesser extent, bax-deficient mice, except that there was no increase in NG2-positive progenitor cells in the dorsal columns of these strains of mutant mice. These increases in mature oligodendrocytes and progenitor cells in bax/bak-deficient mice were unexpectedly proportional to increases in numbers of axons in these white matter tracts, thus retaining the oligodendroglial lineage to axon ratios of at most 1.3-fold of the physiological numbers. This is in contrast to the prominent expansion in numbers of neural precursor cells in the subventricular zones of these adult mutant mice. Our study indicates that homeostatic control of cell number is different for progenitors of the oligodendroglial and neuronal lineages. Furthermore, regulatory mechanism(s) operating in addition to apoptotic elimination through the intrinsic pathway, appear to prevent the overproduction of highly mitotic oligodendroglial progenitor cells.
机译：来自缺乏功能性bax和bak基因的小鼠的高度纯化的少突胶质细胞系细胞在体外分化后对凋亡具有抗性，表明在缺乏神经元（轴突）和其他神经胶质细胞的情况下，固有凋亡途径在少突胶质细胞的凋亡中具有重要作用。因此，这些小鼠提供了有价值的工具，可用来评估内在凋亡通路在调节少突胶质细胞和少突胶质祖细胞的种群大小中的重要性。视神经和脊髓背柱的定量分析表明，成年bax / bak缺陷小鼠的两个白质区中，免疫标记天冬氨酸酰化酶的成熟少突胶质细胞和表达NG2硫酸软骨素蛋白聚糖的成年神经胶质祖细胞的绝对数量均增加。以及bax缺陷型小鼠（程度较小），除了这些突变小鼠株的背侧柱中NG2阳性祖细胞没有增加。 bax / bak缺陷小鼠中成熟的少突胶质细胞和祖细胞的这些增加出乎意料地与这些白质区域中轴突数量的增加成比例，从而使少突胶质细胞系与轴突的比例保持为生理数值的至多1.3倍。这与这些成年突变小鼠的脑室下区域中的神经前体细胞数量的显着增加形成了对比。我们的研究表明，少突胶质细胞和神经元谱系祖细胞对细胞数量的稳态控制是不同的。此外，除了通过内在途径的凋亡消除外，调控机制似乎还可以防止高度有丝分裂的少突胶质祖细胞的过度生产。

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