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Overexpression of Tau Rescues Nogo-66-Induced Neurite Outgrowth Inhibition In Vitro
Yu-Chao Zuo1,2, Hong-Lian Li3, Nan-Xiang Xiong4
1Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Neuroscience Bulletin
|October 21, 2016
Summary
Tau protein overexpression can overcome Nogo-66 inhibition of neurite outgrowth by modulating tau dephosphorylation at S262. This suggests a novel therapeutic target for nerve regeneration.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Nogo-66 inhibits nerve regeneration.
- Tau protein stabilizes microtubules.
- The interaction between Nogo-66 and tau is not fully understood.
Purpose of the Study:
- To investigate the interaction between Nogo-66 and tau.
- To determine if tau can overcome Nogo-66-mediated inhibition of neurite outgrowth.
- To elucidate the role of tau phosphorylation in this process.
Main Methods:
- Overexpression of tau in N2a cells and primary cortical neurons.
- Treatment with Nogo-66 and Hymenialdisine (MARK inhibitor).
- Western blot analysis to quantify protein levels (total tau, phosphorylated tau, MARK).
- Assessment of neurite outgrowth.
Main Results:
- Tau overexpression increased total tau, phosphorylated tau, and MARK levels.
- Nogo-66 increased total tau but decreased p-S262 tau and MARK levels.
- Tau overexpression rescued Nogo-66-induced inhibition of neurite outgrowth.
- MARK inhibition abolished the rescue effect of tau.
Conclusions:
- Dephosphorylation of tau at S262 is crucial for Nogo-66 signaling.
- Tau overexpression can rescue Nogo-66-induced inhibition of neurite outgrowth in vitro.
- Targeting tau phosphorylation may offer a therapeutic strategy for nerve regeneration.
