Neural Regeneration Research ›› 2015, Vol. 10 ›› Issue (9): 1433-1440.doi: 10.4103/1673-5374.165511

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Oxygen-glucose deprivation regulates BACE1 expression through induction of autophagy in Neuro-2a/APP695 cells

Rong-fu Chen1, Ting Zhang1, Yin-yi Sun1, Ya-meng Sun1, Wen-qi Chen1, Nan Shi2, Fang Shen1, Yan Zhang2, Kang-yong Liu1, 2, Xiao-jiang Sun1   

  1. 1 Department of Neurology, Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University, Shanghai, China
    2 Zhoupu Hospital, Pudong New District, Shanghai, China
  • Received:2015-08-05 Online:2015-09-28 Published:2015-09-28
  • Contact: Xiao-jiang Sun, Ph.D., sunxj155@sohu.com.
  • Supported by:

    This work was supported by the National Natural Science Foundation of China, No. 31171014, 31371065; a grant from Shanghai Municipal Health Bureau, China, No. 20134125; a grant from Shanghai Pudong District Health Bureau of China, No. PDZz2013-10

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Abstract:

Our previous findings have demonstrated that autophagy regulation can alleviate the decline of learning and memory by eliminating deposition of extracellular beta-amyloid peptide (Aβ) in the brain after stroke, but the exact mechanism is unclear. It is presumed that the regulation of beta-site APP-cleaving enzyme 1 (BACE1), the rate-limiting enzyme in metabolism of Aβ, would be a key site. Neuro-2a/amyloid precursor protein 695 (APP695) cell models of cerebral ischemia were established by oxygen-glucose deprivation to investigate the effects of Rapamycin (an autophagy inducer) or 3-methyladenine (an autophagy inhibitor) on the expression of BACE1. Either oxygen-glucose deprivation or Rapamycin down-regulated the expression of BACE1 while 3-methyladenine up-regulated BACE1 expression. These results confirm that oxygen-glucose deprivation down-regulates BACE1 expression in Neuro-2a/APP695 cells through the introduction of autophagy.

Key words: nerve regeneration, brain Injury, oxygen-glucose deprivation, cerebral ischemia, stroke, autophagy, beta-site APP-cleaving enzyme 1 (BACE1), beta-amyloid peptide, 3-methyladenine (3-MA), Rapamycin, neural regeneration