Neural Regeneration Research ›› 2013, Vol. 8 ›› Issue (16): 1491-1499.doi: 10.3969/j.issn.2095-4344.2012.33.027

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JNK3 involvement in nerve cell apoptosis and neurofunctional recovery after traumatic brain injury

Jiang Long1, Li Cai1, Jintao Li2, Lei Zhang1, Haiyang Yang1, Tinghua Wang2   

  1. 1 Department of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China
    2 Neuroscience Institute of Kunming Medical University, Kunming 650500, Yunnan Province, China
  • Received:2012-12-07 Revised:2013-03-08 Online:2013-06-05 Published:2013-06-05
  • Contact: Jiang Long☆, M.D., Associate chief physician, Department of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China, longjiang69@163.com. Tinghua Wang, M.D., Professor, Neuroscience Institute of Kunming Medical University, Kunming 650500, Yunnan Province, China, tinghua_neuron@263.net.
  • About author:Jiang Long and Li Cai contributed equally to this work

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Abstract:

Increasing evidence has revealed that the activation of the JNK pathway participates in apoptosis of nerve cells and neurological function recovery after traumatic brain injury. However, which genes in the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in cell apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1, 3, 5, 14 and 28 days post injury. These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury.

Key words: neural regeneration, JNK1, JNK2, JNK3, traumatic brain injury, TdT-mediated dUTP nick end labeling, reverse transcription-PCR, cell apoptosis, neurological function recovery, neuroregeneration