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Robust Neuritogenesis-Promoting Activity by Bis(heptyl)-Cognitin Through the Activation of alpha7-Nicotinic Acetylcholine Receptor/ERK Pathway
Hu S.-Q.1,2,3; Cui W.1,3; Mak S.-H.1,3; Choi C.-L.1; Hu Y.-J.4; Li G.5; Tsim K.W.-K.6; Pang Y.-P.7; Han Y.-F.1,3
2015-06-01
Source PublicationCNS Neuroscience and Therapeutics
ISSN17555949 17555930
Volume21Issue:6Pages:520-529
Other 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 μM) 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 β-III-tubulin-positive neurites. Furthermore, B7C rapidly increased ERK phosphorylation. Specific inhibitors of alpha7-nicotinic acetylcholine receptor (α7-nAChR) and MEK, but not those of p38 or JNK, blocked the neurite outgrowth as well as ERK phosphorylation induced by B7C. Most importantly, genetic depletion of α7-nAChR significantly abolished B7C-induced neurite outgrowth in PC12 cells. Conclusion: B7C promoted neurite outgrowth through the activation of α7-nAChR/ERK pathway, which offers novel insight into the potential application of B7C in the treatment of neurodegenerative disorders.

KeywordAlpha7-nicotinic Acetylcholine Receptor Bis(Heptyl)-cognitin Extracellular Signal-regulated Kinase Neurite Outgrowth Neurodegenerative Disorders
DOI10.1111/cns.12401
URLView the original
Language英語English
WOS Research AreaNeurosciences & Neurology ; Pharmacology & Pharmacy
WOS SubjectNeurosciences ; Pharmacology & Pharmacy
WOS IDWOS:000354646500006
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Cited Times [WOS]:9   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
Corresponding AuthorHan Y.-F.
Affiliation1.Department of Applied Biology and Chemical Technology, Institute of Modern Chinese Medicine, The Hong Kong Polytechnic University, Hung Hom,Hong Kong, China
2.Institute of New Drug Research, Guangdong Province Key Laboratory of Pharmacodynamic, Constituents of Traditional Chinese Medicine & NewDrug Research, College of Pharmacy, Jinan University, Guangdong, China
3.The Hong Kong Polytechnic University Shenzhen Research Institute, Shenzhen, China
4.State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau, China
5.National Engineering Laboratory for Modern Silk, College of Textile and Clothing Engineering, Soochow University, Suzhou, China
6.Division of Life Science and Center for Chinese Medicine, The Hong Kong University of Science and Technology, Hong Kong, China
7.Mayo Cancer Center, Department of Pharmacology, Mayo Clinic, Rochester, MN, USA
Recommended Citation
GB/T 7714
Hu S.-Q.,Cui W.,Mak S.-H.,et al. Robust Neuritogenesis-Promoting Activity by Bis(heptyl)-Cognitin Through the Activation of alpha7-Nicotinic Acetylcholine Receptor/ERK Pathway[J]. CNS Neuroscience and Therapeutics,2015,21(6):520-529.
APA Hu S.-Q.,Cui W.,Mak S.-H.,Choi C.-L.,Hu Y.-J.,Li G.,Tsim K.W.-K.,Pang Y.-P.,&Han Y.-F..(2015).Robust Neuritogenesis-Promoting Activity by Bis(heptyl)-Cognitin Through the Activation of alpha7-Nicotinic Acetylcholine Receptor/ERK Pathway.CNS Neuroscience and Therapeutics,21(6),520-529.
MLA Hu S.-Q.,et al."Robust Neuritogenesis-Promoting Activity by Bis(heptyl)-Cognitin Through the Activation of alpha7-Nicotinic Acetylcholine Receptor/ERK Pathway".CNS Neuroscience and Therapeutics 21.6(2015):520-529.
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