Mitogen Activated Protein Kinase Family Proteins and c-jun Signaling in Injury-induced Schwann Cell Plasticity.
Mitogen Activated Protein Kinase Family Proteins and c-jun Signaling in Injury-induced Schwann Cell Plasticity.
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DOI：
10.5607/en.2014.23.2.130
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发表时间：
2014-06
影响因子：
2.4
通讯作者：
Park HT
中科院分区：
文献类型：
--
作者：
Lee HJ;Shin YK;Park HT
周围神经中的雪旺细胞（SC）在出生后发育期间使轴突形成髓鞘，以允许神经冲动的跳跃式传导。除非神经受到损伤，否则髓鞘的良好组织结构在整个生命过程中得以维持。周围神经损伤后，来自损伤神经的未知信号驱动SC去分化成未成熟状态。去分化的SC通过产生神经营养因子和清除退化的神经碎片参与轴突再生。本文就丝裂原活化蛋白激酶家族蛋白（MAP激酶）在SC去分化中的作用作一综述。此外，我们将突出神经调节蛋白1和转录因子c-jun作为上游和下游信号的MAP激酶在SC神经损伤的反应。
Schwann cells (SCs) in the peripheral nerves myelinate axons during postnatal development to allow saltatory conduction of nerve impulses. Well-organized structures of myelin sheathes are maintained throughout life unless nerves are insulted. After peripheral nerve injury, unidentified signals from injured nerves drive SC dedifferentiation into an immature state. Dedifferentiated SCs participate in axonal regeneration by producing neurotrophic factors and removing degenerating nerve debris. In this review, we focus on the role of mitogen activated protein kinase family proteins (MAP kinases) in SC dedifferentiation. In addition, we will highlight neuregulin 1 and the transcription factor c-jun as upstream and downstream signals for MAP kinases in SC responses to nerve injury.