Neural Regeneration Research ›› 2016, Vol. 11 ›› Issue (1): 114-118.doi: 10.4103/1673-5374.175055

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Specific effects of c-Jun NH2-terminal kinase-interacting protein 1 in neuronal axons

Shu Tang 1, Qiang Wen 2, Xiao-jian Zhang 1, Quan-cheng Kan 1   

  1. 1 Department of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China
    2 Department of Clinical Pharmacology, Basic Medical College, Zhengzhou University, Zhengzhou, Henan Province, China
  • Received:2015-10-26 Online:2016-01-15 Published:2016-01-15
  • Contact: Shu Tang, M.D.,tangshu018@163.com.
  • Supported by:

    This study was supported by the Henan Province Education Department Key Project of Science and Technology Research in China, No. 12A350006.

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Abstract:

c-Jun NH2-terminal kinase (JNK)-interacting protein 3 plays an important role in brain-derived neurotrophic factor/tropomyosin-related kinase B (TrkB) anterograde axonal transport. It remains unclear whether JNK-interacting protein 1 mediates similar effects, or whether JNK-interacting protein 1 affects the regulation of TrkB anterograde axonal transport. In this study, we isolated rat embryonic hippocampus and cultured hippocampal neurons in vitro. Coimmunoprecipitation results demonstrated that JNK-interacting protein 1 formed TrkB complexes in vitro and in vivo. Immunocytochemistry results showed that when JNK-interacting protein 1 was highly expressed, the distribution of TrkB gradually increased in axon terminals. However, the distribution of TrkB reduced in axon terminals after knocking out JNK-interacting protein 1. In addition, there were differences in distribution of TrkB after JNK-interacting protein 1 was knocked out compared with not. However, knockout of JNK-interacting protein 1 did not affect the distribution of TrkB in dendrites. These findings confirm that JNK-interacting
protein 1 can interact with TrkB in neuronal cells, and can regulate the transport of TrkB in axons, but not in dendrites.

Key words: nerve regeneration, c-Jun NH2-terminal kinase-interacting protein, neurons, brain-derived neurotrophic factor, tropomyosin-related kinase B, axons, hippocampus, dendrites, regulation, neural regeneration