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Reduction and the intracellular translocation of EphB2 in Tg2576 mice and the effects of β-amyloid

Authors

  • M. Qu,

    1. Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
    2. Key Laboratory of Neurological Diseases of Education Ministry of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
    3. Hubei Provincial Center for Disease Control and Prevention, Wuhan, China
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    • These authors contributed equally.
  • J. Jiang,

    1. Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
    2. Key Laboratory of Neurological Diseases of Education Ministry of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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    • These authors contributed equally.
  • X-P. Liu,

    1. Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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  • Q. Tian,

    1. Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
    2. Key Laboratory of Neurological Diseases of Education Ministry of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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  • L-M. Chen,

    1. Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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  • G. Yin,

    1. Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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  • D. Liu,

    1. Department of Genetics, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
    2. Key Laboratory of Neurological Diseases of Education Ministry of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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  • J-Z. Wang,

    Corresponding author
    1. Key Laboratory of Neurological Diseases of Education Ministry of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
    • Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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  • L-Q. Zhu

    Corresponding author
    1. Key Laboratory of Neurological Diseases of Education Ministry of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
    • Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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Correspondence: Ling-Qiang Zhu or Jian-Zhi Wang, Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Tel: +86 27 8369 2625; Fax: +86 27 8369 3883; E-mail: zhulq@mail.hust.edu.cn or wangjz@mails.tjmu.edu.cn

Abstract

Aims

EphB2 is a member of receptor tyrosine kinases (RTKs) family that is essential for the cell adhesion, neural crest migration, axon guidance and synaptogenesis in the nervous system. Recent studies show that preservation of EphB2 in a transgenic mouse model of Alzheimer's disease (AD) rescues the cognitive deficit, suggesting a crucial role of EphB2 in AD. However, the expression and distribution profiles of EphB2 in the early stage of AD have not been reported.

Methods

Immunohistochemistry, immunoblot and immunofluorescence were used to analyse the level of EphB2 in Tg2576 mice at different ages and in cultured neurones with Aβ treatment at different times.

Results

EphB2 was reduced in an age-dependent manner in the olfactory bulb and the hippocampus of Tg2576 mice. The decrease of EphB2 appeared earlier in the olfactory bulb than the hippocampus, and reduction of EphB2 appeared earlier than that of MAP2, a dendritic cytoskeleton marker. In the cortex, EphB2 displayed a significant translocation from the neuronal processes to the cell bodies with ageing. In primary hippocampal neuronal cultures, Aβ42 treatment also induced the decrement of EphB2 that was prior to the decline of MAP2.

Conclusions

Our findings provide the first evidence for an age- and region-dependent reduction and intracellular translocation of EphB2 in Tg2576 mice, and the foremost decrement of EphB2 in the olfactory bulb may represent an early sign of AD.

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