β1-integrin signaling mediates premyelinating oligodendrocyte survival but is not required for CNS myelination and remyelination
β1-integrin signaling mediates premyelinating oligodendrocyte survival but is not required for CNS myelination and remyelination
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DOI：
10.1523/jneurosci.0444-06.2006
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发表时间：
2006-07-19
影响因子：
5.3
通讯作者：
Relvas, Joao B.
中科院分区：
文献类型：
--
作者：
Benninger, Yves;Colognato, Holly;Relvas, Joao B.
之前的报道，包括在少突胶质细胞祖细胞中使用显性失活抑制β1-整合素信号传导的移植实验，表明β1-整合素信号传导是髓鞘形成所必需的。在这里，我们利用中枢神经系统发育过程中少突胶质细胞中 β1-整合素基因的条件消融来检验这一假设。这种方法使我们能够研究中枢神经系统生理环境中的少突胶质细胞β1-整合素信号传导，避免了显性失活方法的潜在缺点。我们发现β1-整合素信号传导的作用比之前预期的要有限得多。尽管β1-整合素信号参与阶段特异性少突胶质细胞的存活，但轴突鞘和髓鞘形成本身并不需要β1-整合素信号传导。我们还发现，在脊髓中，髓鞘再生在缺乏 β1-整合素的情况下正常发生。我们的结论是，虽然β1-整合素可能仍然对少突胶质细胞生物学的其他方面有贡献，但它对于中枢神经系统中的髓鞘形成和髓鞘再生来说并不是必需的。
Previous reports, including transplantation experiments using dominant-negative inhibition of beta 1-integrin signaling in oligodendrocyte progenitor cells, suggested that beta 1-integrin signaling is required for myelination. Here, we test this hypothesis using conditional ablation of the beta 1-integrin gene in oligodendroglial cells during the development of the CNS. This approach allowed us to study oligodendroglial beta 1-integrin signaling in the physiological environment of the CNS, circumventing the potential drawbacks of a dominant-negative approach. We found that beta 1-integrin signaling has a much more limited role than previously expected. Although it was involved in stage-specific oligodendrocyte cell survival, beta 1-integrin signaling was not required for axon ensheathment and myelination per se. We also found that, in the spinal cord, remyelination occurred normally in the absence of beta 1-integrin. We conclude that, although beta 1-integrin may still contribute to other aspects of oligodendrocyte biology, it is not essential for myelination and remyelination in the CNS.