Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/21051
Title: Robust Neuritogenesis-Promoting Activity by Bis(heptyl)-Cognitin Through the Activation of alpha7-Nicotinic Acetylcholine Receptor/ERK Pathway
Authors: Hu, SQ
Cui, W
Mak, SH
Choi, CL
Hu, YJ
Li, G
Tsim, KWK
Pang, YP
Han, YF 
Keywords: Alpha7-nicotinic acetylcholine receptor
Bis(heptyl)-cognitin
Extracellular signal-regulated kinase
Neurite outgrowth
Neurodegenerative disorders
Issue Date: 2015
Publisher: Blackwell Publishing Ltd
Source: CNS Neuroscience and Therapeutics, 2015, v. 21, no. 6, p. 520-529 How to cite?
Journal: CNS Neuroscience and Therapeutics 
Abstract: Aims: Neurodegenerative disorders are caused by progressive neuronal loss in the brain, and hence, compounds that could promote neuritogenesis may have therapeutic values. In this study, the effects of bis(heptyl)-cognitin (B7C), a multifunctional dimer, on neurite outgrowth were investigated in both PC12 cells and primary cortical neurons. Methods: Immunocytochemical staining was used to evaluate the proneuritogenesis effects, and Western blot and short hairpin RNA assays were applied to explore the underlying mechanisms. Results: B7C (0.1-0.5 £gM) induced robust neurite outgrowth in PC12 cells, as evidenced by the neurite-bearing morphology and upregulation of growth-associated protein-43 expression. In addition, B7C markedly promoted neurite outgrowth in primary cortical neurons as shown by the increase in the length of £]-III-tubulin-positive neurites. Furthermore, B7C rapidly increased ERK phosphorylation. Specific inhibitors of alpha7-nicotin
URI: http://hdl.handle.net/10397/21051
ISSN: 1755-5930
DOI: 10.1111/cns.12401
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