NDLI: Wnt / ß-Catenin Signaling Pathway Against Aβ Toxicity in PC12 Cells.

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Wnt / ß-Catenin Signaling Pathway Against Aβ Toxicity in PC12 Cells.

Content Provider	Semantic Scholar
Author	Zheng, Yaping Wang, Jin Li, Deheng Guo, Meixia Zhen, Minghui Chang, Quanzhong
Copyright Year	2016
Abstract	BACKGROUND/AIMS Alzheimer's disease (AD) is characterized by accumulation of β-amyloid (Aβ), However, the mechanism of how Aβ affects neuronal cell death remains elusive. The balance of pro- and anti-apoptotic Bcl-2 family proteins (e.g., Bcl-2 and Bax) has been known to play a pivotal role in neuronal cell death. Of note, expression levels of these proteins are changed in the neurons in AD. To date no study has elusidated the relationship between Aβ and Bax. METHODS The present study explored the role of Wnt/β-catenin pathway in the neurotoxic effect of Aβ25-35. Flow cytometry was employed to determine the apoptosis, western blotting to assess the protein abundance of Bcl-2 and BAX, MTT assay to decipher the cells viability. RESULTS As a result, the addition of Wnt3a significantly prevented oligomeric Aβ-induced neuronal cell death and viability. Furthermore, treatment with Aβ25-35 increased Bax and Bcl-2 protein abundance and mRNA levels, an effect significantly blocked by Wnt3a (100 ng/ml) and GSK3β inhibitor TWS119 (10µM). CONCLUSION These findings are first to demonstrate that Wnt/β-catenin signaling pathway regulates Aβ25-35-induced apoptosis.
Starting Page	40
Ending Page	47
Page Count	8
File Format	PDF HTM / HTML
Alternate Webpage(s)	https://www.karger.com/Article/Pdf/442610
PubMed reference number	27318974v1
Alternate Webpage(s)	https://doi.org/10.1159/000442610
DOI	10.1159/000442610
Journal	Neuro-Signals
Volume Number	24
Issue Number	1
Language	English
Access Restriction	Open
Subject Keyword	Alzheimer's Disease Apoptosis BCL2 gene Catenins Cell Death Neurotoxicity Syndromes Signal Transduction Pathways WNT3A gene Western Blotting monooxyethylene trimethylolpropane tristearate neuron death
Content Type	Text
Resource Type	Article

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