Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (5): 519-525.doi: 10.4103/1673-5374.130079

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Transient axonal glycoprotein-1 induces apoptosis-related gene expression without triggering apoptosis in U251 glioma cells

Haigang Chang 1, 2, Shanshan Song 3, Zhongcan Chen 2, Yaxiao Wang 1, Lujun Yang 2, Mouxuan Du 2, Yiquan Ke 2, Ruxiang Xu 4, Baozhe Jin 1, Xiaodan Jiang 2   

  1. 1 Department of Neurosurgery, the First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan Province, China
    2 Neurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong Province, Department of Neurosurgery, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China
    3 Eight-year Programme, the First Clinical Medical College of Southern Medical University, Guangzhou, Guangdong Province, China
    4 Department of Neurosurgery, Military General Hospital of Beijing PLA, Beijing, China
  • Received:2014-02-07 Online:2014-03-12 Published:2014-03-12
  • Contact: Baozhe Jin, M.D., Department of Neurosurgery, the First Affiliated Hospital of Xinxiang Medical University, Weihui 453100, Henan Province, China, 13938765496@ 163.com. Xiaodan Jiang, M.D., Ph.D., Neurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong Province, Department of Neurosurgery, Zhujiang Hospital of Southern Medical University, Guangzhou 510282, Guangdong Province, China, jiangxiao_dan@163.com.
  • Supported by:

    This work was supported by grants from the National Natural Science Foundation of China, No. 81171179, 81272439; the Key Sci-Tech Research Projects of Guangdong Province in China, No. 2008A030201019; and the Guangzhou Municipal Science and Technology Project in China, No. 09B52120112-2009J1-C418-2, No. 2008A1-E4011-6.

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Abstract:

Previous studies show that transient axonal glycoprotein-1, a ligand of amyloid precursor protein, increases the secretion of amyloid precursor protein intracellular domain and is involved in apoptosis in Alzheimer’s disease. In this study, we examined the effects of transient axonal glycoprotein-1 on U251 glioma cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed that transient axonal glycoprotein-1 did not inhibit the proliferation of U251 cells, but promoted cell viability. The terminal deoxynucleotidyl transferase dUTP nick end labeling assay showed that transient axonal glycoprotein-1 did not induce U251 cell apoptosis. Real-time PCR revealed that transient axonal glycoprotein-1 substantially upregulated levels of amyloid precursor protein intracellular C-terminal domain, and p53 and epidermal growth factor receptor mRNA expression. Thus, transient axonal glycoprotein-1 increased apoptosis-related gene expression in U251 cells without inducing apoptosis. Instead, transient axonal glycoprotein-1 promoted the proliferation of these glioma cells.

Key words: nerve regeneration, brain injury, glioma cells, transient axonal glycoprotein-1, APP intracellular domain, p53, epidermal growth factor receptor, NSFC grant, neural regeneration