Oxygen-glucose deprivation regulates BACE1 expression through induction of autophagy in Neuro-2a/APP695 cells
- Resource Type
- Authors
- Nan Shi; Rongfu Chen; Ting Zhang; Fang Shen; Yameng Sun; Wenqi Chen; Kangyong Liu; Yan Zhang; Xiaojiang Sun; Yinyi Sun
- Source
- Neural Regeneration Research
Neural Regeneration Research, Vol 10, Iss 9, Pp 1433-1440 (2015)
- Subject
- oxygen-glucose deprivation
autophagy
Cell
Ischemia
lcsh:RC346-429
cerebral ischemia
Developmental Neuroscience
mental disorders
medicine
Extracellular
Amyloid precursor protein
Inducer
3-methyladenine (3-MA)
Rapamycin
nerve regeneration
lcsh:Neurology. Diseases of the nervous system
chemistry.chemical_classification
brain Injury
biology
business.industry
Autophagy
beta-site APP-cleaving enzyme 1 (BACE1)
Metabolism
medicine.disease
stroke
Cell biology
Enzyme
medicine.anatomical_structure
chemistry
biology.protein
business
beta-amyloid peptide
neural regeneration
Neuroscience
Research Article
- Language
- English
- ISSN
- 1876-7958
1673-5374
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.