NDLI: Nicotine Decreases Beta-Amyloid Through Regulating BACE1 Transcription in SH-EP1-α4β2 nAChR-APP695 Cells

Content Provider	Springer Nature Link
Author	Nie, Hui Zhen Li, Zuo Qing Yan, Qi Xin Wang, Ze Jian Zhao, Wen Juan Guo, Ling Chen Yin, Ming
Copyright Year	2011
Abstract	Alzheimer’s disease (AD) is a neurodegenerative disorder that affects the elderly population. Deposition of beta-amyloid (Aβ) in the brain is a hallmark of AD pathology. In our previous study, we have constructed a cell line expressing human APP695 (hAPP695) in SH-EP1 cells stably transfected with human nicotinic receptor (nAChR) α4 subunit and β2 subunit gene. In present study, we found that activation of α4β2 nAChR by nicotine and epibatidine decreased secreted Aβ level in the cell line and hippocampal neurons, but had no effects on full-length APP695 and sAPP-α. Nicotine also decreases BACE1 and PSEN1 expression, as well as ERK1 and NFκB P65 subunit expression in the cell line. Furthermore, BACE1 promoter activity is, but PSEN1 not, decreased by nicotine in the cell line. All the results suggest that activation of α4β2 nAChR decreases Aβ through regulating BACE1 transcription by ERK1-NFκB pathway. Additionally, analysis of BACE1 promoter activity by dual-luciferase reporter assay may be useful for drug screening as a high throughput method.
Starting Page	904
Ending Page	912
Page Count	9
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	36
Issue Number	5
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2011-02-19
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Alzheimer’s disease Beta-amyloid BACE1 nAChR Cell Biology Neurosciences Neurochemistry Biochemistry Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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Construction of SH-EP1-α4β2-hAPP695 Cell Line and Effects of Nicotinic Agonists on β-amyloid in the Cells

Epigallocatechin Gallate Attenuates β-Amyloid Generation and Oxidative Stress Involvement of PPARγ in N2a/APP695 Cells

Activation of Liver X Receptor Decreases BACE1 Expression and Activity by Reducing Membrane Cholesterol Levels

Sphingosylphosphorylcholine Attenuated β–Amyloid Production by Reducing BACE1 Expression and Catalysis in PC12 Cells

Effects of Edaravone on Amyloid-β Precursor Protein Processing in SY5Y-APP695 Cells

The Neuroprotective Effects of Justicidin A on Amyloid Beta$_{25–35}$-Induced Neuronal Cell Death Through Inhibition of Tau Hyperphosphorylation and Induction of Autophagy in SH-SY5Y Cells

Tripchlorolide Attenuates β-amyloid Generation via Suppressing PPARγ-Regulated BACE1 Activity in N2a/APP695 Cells

Characterization of Human α4β2 Neuronal Nicotinic Receptors Stably Expressed in SH-EP1 Cells

Amyloid-β Production: Major Link Between Oxidative Stress and BACE1

Nicotine Decreases Beta-Amyloid Through Regulating BACE1 Transcription in SH-EP1-α4β2 nAChR-APP695 Cells

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