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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The cyclin-dependent kinase inhibitor p57kip2 is a negative regulator of Schwann cell differentiation and in vitro myelination
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The cyclin-dependent kinase inhibitor p57kip2 is a negative regulator of Schwann cell differentiation and in vitro myelination

机译：细胞周期蛋白依赖性激酶抑制剂p57kip2是雪旺氏细胞分化和体外髓鞘形成的负调节剂

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摘要

The p57kip2 gene encodes a member of the cyclin-dependent kinase inhibitor family, proteins known to block G_1/S transition during the mammalian cell cycle. We observed that expression of p57kip2 in Schwann cells of the developing and injured adult peripheral nervous system is dynamically regulated. Using gene knockdown by means of vector-based RNA interference in cultured primary Schwann cells we found that reduced levels of p57kip2 lead to cell cycle exit, actin filament stabilization, altered cell morphology and growth, and down-regulation of promyelinating markers as well as induction of myelin genes and proteins. In addition, we could demonstrate that in vitro myelination is enhanced by p57kip2-suppressed Schwann cells. Using microarray technology we found that these cellular reactions are specific to lowered p57kip2 expression levels and detected a shift of the transcriptional expression program toward the pattern known from Schwann cells in developing peripheral nerves. Because in the absence of axons primary Schwann cells normally do not display differentiation-associated reactions, we conclude that we have identified a mechanism and an important intrinsic negative regulator of myelinating glia differentiation.
机译：p57kip2基因编码细胞周期蛋白依赖性激酶抑制剂家族的成员，该蛋白已知在哺乳动物细胞周期中会阻止G_1 / S过渡。我们观察到，p57kip2在发育中和受损的成人周围神经系统的雪旺细胞中的表达是动态调节的。利用基于载体的RNA干扰在培养的Schwann原代细胞中进行基因敲除，我们发现降低的p57kip2水平可导致细胞周期退出，肌动蛋白丝稳定，细胞形态和生长改变以及早髓鞘标记物的下调以及诱导髓磷脂基因和蛋白质。此外，我们可以证明p57kip2抑制的雪旺细胞可增强体外髓鞘形成。使用微阵列技术，我们发现这些细胞反应对降低的p57kip2表达水平具有特异性，并检测到转录表达程序朝着发育中的神经中雪旺氏细胞已知模式的转移。因为在没有轴突的情况下，原代施万细胞通常不显示分化相关反应，所以我们得出的结论是，我们已经确定了髓鞘胶质细胞分化的机制和重要的内在负调节剂。

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