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Exp Neurobiol 2014; 23(2): 130-137
Published online June 30, 2014
https://doi.org/10.5607/en.2014.23.2.130
© The Korean Society for Brain and Neural Sciences
Hye Jeong Lee1, Yoon Kyung Shin2 and Hwan Tae Park2*
Departments of 1Pharmacology and 2Physiology, Mitochondria Hub Regulation Center (MHRC), College of Medicine, Dong-A University, Busan 602-714, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-51-240-2636, FAX: 82-51-247-3318
e-mail: phwantae@dau.ac.kr
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.
Keywords: Schwann cell, dedifferentiation, plasticity, nerve injury, mitogen activated protein kinase family proteins, c-jun