首页> 美国卫生研究院文献>The Journal of Neuroscience >β1-Integrin Signaling Mediates Premyelinating Oligodendrocyte Survival But Is Not Required for CNS Myelination and Remyelination
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β1-Integrin Signaling Mediates Premyelinating Oligodendrocyte Survival But Is Not Required for CNS Myelination and Remyelination

机译:β1-整合素信号传导介导前髓鞘少突胶质细胞的存活但对于中枢神经系统髓鞘再生和髓鞘再生并不需要

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摘要

Previous reports, including transplantation experiments using dominant-negative inhibition of β1-integrin signaling in oligodendrocyte progenitor cells, suggested that β1-integrin signaling is required for myelination. Here, we test this hypothesis using conditional ablation of the β1-integrin gene in oligodendroglial cells during the development of the CNS. This approach allowed us to study oligodendroglial β1-integrin signaling in the physiological environment of the CNS, circumventing the potential drawbacks of a dominant-negative approach. We found that β1-integrin signaling has a much more limited role than previously expected. Although it was involved in stage-specific oligodendrocyte cell survival, β1-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 β1-integrin. We conclude that, although β1-integrin may still contribute to other aspects of oligodendrocyte biology, it is not essential for myelination and remyelination in the CNS.
机译:以前的报道,包括在少突胶质细胞祖细胞中使用显性阴性抑制β1-整合素信号转导的移植实验,都表明β1-整联蛋白信号是髓鞘化所必需的。在这里,我们使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在中枢神经系统的生理环境中研究少突胶质β1-整合素信号转导,从而避免了显性阴性方法的潜在弊端。我们发现,β1-整联蛋白信号传导的作用比以前预期的要有限得多。尽管它参与了特定阶段的少突胶质细胞的存活,但是β1-整合素信号转导本身对于轴突的包被和髓鞘形成并不是必需的。我们还发现,在脊髓中,在没有β1-整联蛋白的情况下正常发生髓鞘再生。我们得出的结论是,尽管β1-整合素可能仍然有助于少突胶质细胞生物学的其他方面,但对于中枢神经系统的髓鞘化和再髓鞘化并不是必需的。

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