Neural Regeneration Research ›› 2012, Vol. 7 ›› Issue (26): 2005-2011.

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P75 and phosphorylated c-Jun are differentially regulated in spinal motoneurons following axotomy in rats

Qiuju Yuan1, Huanxing Su2, Wutian Wu 2-5, Zhi-Xiu Lin1   

  1. 1 School of Chinese Medicine, Faculty of Science, the Chinese University of Hong Kong, Shatin, N.T, Hong Kong Special Administrative Region, China
    2 Department of Anatomy, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region, China
    3 State Key Laboratory of Brain and Cognitive Sciences, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region, China
    4 Research Center of Reproduction, Development and Growth, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region, China
    5 Joint Laboratory for Brain Function and Health (BFAH), Jinan University and the University of Hong Kong, Guangzhou, China
  • Received:2012-05-11 Revised:2012-07-10 Online:2012-09-15 Published:2012-09-15
  • Contact: Zhi-Xiu Lin, Ph.D., School of Chinese Medicine, Faculty of Science, the Chinese University of Hong Kong, Shatin, N.T, Hong Kong Special Administrative Region, China; Wutian Wu, Department of Anatomy, Li Ka Shing Faculty of Medicine, the University of Hong Kong, 21 Sassoon Road, Hong Kong Special Administrative Region, China. linzx@cuhk.edu.hk wtwu@hkucc.hku.hk
  • About author:Qiuju Yuan☆, Ph.D., School of Chinese Medicine, Faculty of Science, the Chinese University of Hong Kong, Shatin, N.T, Hong Kong Special Administrative Region, China

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Abstract:

The neurotrophin receptor (p75) activates the c-Jun N-terminal kinase (JNK) pathway. Activation of JNK and its substrate c-Jun can cause apoptosis. Here we evaluate the role of p75 in spinal motoneurons by comparing immunoreactivity for p75 and phosphorylated c-Jun (p-c-Jun), the production of JNK activation in axotomized motoneurons in postnatal day (PN)1, PN7, PN14 and adult rats. Intensive p-c-Jun was induced in axotomized motoneurons in PN1 and PN7. In PN14, p-c-Jun expression was sharply reduced after the same injury. The decreased expression of p-c-Jun at this age coincided with a developmental switch of re-expression of p75 in axotomized cells. In adult animals, no p-c-Jun but intensive p75 was detected in axotomized motoneurons. These results indicate differential expression or turnover of phosphorylation of c-Jun and p75 in immature versus mature spinal motoneurons in response to axonal injury. The non-co-occurrence of p75 and p-c-Jun in injured motoneurons indicated that p75 may not activate JNK pathway, suggesting that the p75 may not be involved in cell death in axotomized motoneurons.

Key words: apoptosis, transcription factor, c-Jun N-terminal kinase, nerve growth factor receptor, motoneuron, spinal cord, axotomy, neonatal, adult, axonal regeneration