Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (21): 1923-1928.doi: 10.4103/1673-5374.145362

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Amyloid precursor-like protein 2 C-terminal fragments upregulate S100A9 gene and protein expression in BV2 cells

Guangzhe Li 1, Hui Chen 2, Lin Cheng 2, Rongjie Zhao 3, Junchang Zhao 3, Yanji Xu 2   

  1. 1 Department of Psychology, Yanbian Brain Hospital, Yanji, Jilin Province, China
    2 Department of Preventive Medicine, Medical College, Yanbian University, Yanji, Jilin Province, China
    3 Department of Pharmacology, Mudanjiang Medical University, Mudanjiang, Heilongjiang, China
  • Received:2014-09-06 Online:2014-11-15 Published:2014-11-15
  • Contact: Yanji Xu, Ph.D., Department of Preventive Medicine, Medical College, Yanbian University, Yanji 133002, Jilin Province, China, xuyanji@ybu.edu.cn.
  • Supported by:

    This work was supported by the Natural Science Foundation of Technology Gallery in Jilin Province of China, No. 2011-15237; and the National Natural Science Foundation of China, No. 81160159.

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Abstract:

The murine microglial cell line BV2 has neuroprotective effects, but is toxic to neurons by secreting inflammatory cytokines, and is an important target in the treatment of nerve inflammation and neurodegenerative diseases. In the present study, we observed the effects of transfecting three amyloid precursor-like protein 2 (APLP2) C-terminal fragments (CTFs; C57, C50 and C31) in the pEGFP-N1 vector on S100A9 expression in BV2 cells. Reverse transcription-PCR, western blot assay and immunocytochemistry revealed that S100A9 protein and mRNA expression was greater in BV2 cells after CTF transfection than after mock transfection with an empty vector. Furthermore, transfection of full-length APLP2-751 resulted in low levels of S100A9 protein expression. Our results show that APLP2-CTFs upregulate S100A9 protein and mRNA expression in BV2 cells, and identify a novel pathway involved in neuronal injury and apoptosis, and repair and protection in Alzheimer’s disease.

Key words: nerve regeneration, neurodegeneration, Alzheimer’s disease, APLP2, S100A9, C-terminal fragments, amyloid precursor protein, BV2 cells, γ-secretase, NSFC grant, neural regeneration