Abstract | BACKGROUND: METHODS: We set up the culture of primary mouse neurons in vitro and manipulated the expression level of NMNAT1 by RNA interference and gene overexpression methods. Using electroporation transfection we can up-regulate or down-regulate NMNAT1 in cultured mouse dendrites and axons and study the neuronal morphogenesis by immunocytochemistry. In all functional assays, FK-866 (CAS 658084-64-1), a highly specific non-competitive inhibitor of nicotinamide phosphoribosyltransferase was used as a pharmacological and positive control. RESULTS: Our results showed that knocking down NMNAT1 by RNA interference led to a marked decrease in dendrite outgrowth and branching and a significant decrease in axon growth and branching in developing cortical neurons in vitro. CONCLUSIONS: These findings reveal a novel role for NMNAT1 in the morphogenesis of developing cortical neurons, which indicate that the loss of function of NMNAT1 may contribute to different neurodegenerative disorders in central nervous system.
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Authors | Hong Zhao, Jing-Yu Zhang, Zi-Chao Yang, Ming Liu, Bao-Zhi Gang, Qing-Jie Zhao |
Journal | Chinese medical journal
(Chin Med J (Engl))
Vol. 124
Issue 20
Pg. 3373-7
(Oct 2011)
ISSN: 2542-5641 [Electronic] China |
PMID | 22088538
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Nicotinamide-Nucleotide Adenylyltransferase
- Nmnat1 protein, mouse
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Topics |
- Animals
- Axons
(metabolism)
- Blotting, Western
- Cells, Cultured
- Dendrites
(metabolism)
- Immunohistochemistry
- Mice
- Morphogenesis
(genetics, physiology)
- Neurons
(cytology, metabolism)
- Nicotinamide-Nucleotide Adenylyltransferase
(genetics, metabolism)
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