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

作　　者：Qiuju Yuan Huanxing Su Wutian Wu Zhi-Xiu Lin 

机构地区：[1]School of Chinese Medicine, Faculty of Science, the Chinese University of Hong Kong, Shatin, N. T, Hong Kong Special AdministrativeRegion, China [2]Department ofAnatomy, 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 ofHong Kong, Pokfulam, Hong KongSpecial Administrative Region, China [4]Research Center of Reproduction, Development and Growth, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Pokfulam, HongKoncl Special Administrative Reqion, China [5]Joint Laboratory for Brain Function and Health (BFAH), Jinan University and the University of Hong Kong, Guangzhou, China

出　　处：《Neural Regeneration Research》2012年第26期2005-2011,共7页中国神经再生研究（英文版）

基　　金：supported by Direct Grant (Project No.2030392) of the Chinese University of Hong Kong;HK Spinal Cord Injury Foundation;National Key Basic Research Support Foundation (973 Project: 2011CB504402)

摘　　要：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）I, 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.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）I, 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.

关 键 词：apoptosis transcription factor c-Jun N-terminal kinase nerve growth factor receptor MOTONEURON spinal cord AXOTOMY NEONATAL adult axonal regeneration 

分 类 号：Q813.11[生物学—生物工程] Q492.4