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Klf2-Vav1-Rac1 axis promotes axon regeneration after peripher
Custom-Made AAVs were used for gene over-expression and knockdown. (From BrainVTA)
The viruses used in this article from BrainVTA are in the table below
Custom-Made AAV  AAV2/8-CMV-Vav1
 AAV2/8-U6-Loxp-CMV-EGFP-Loxp-Vav1 shRNA-SV40 pA
Qihui Wang, Leilei Gong, Susu Mao, Chun Yao, Mingwen Liu, Yaxian Wang, Jian Yang, Bin Yu, Guiquan Chen, Xiaosong Gu
Pub Date: 2021-06-18, DOI: 10.1016/j.expneurol.2021.113788, Email: [email protected]
Increasing the intrinsic regeneration potential of neurons is the key to promote axon regeneration and repair of nerve injury. Therefore, identifying the molecular switches that respond to nerve injury may play critical role in improving intrinsic regeneration ability. The mechanisms by which injury unlocks the intrinsic axonal growth competence of mature neurons are not well understood. The present study identified the key regulatory genes after sciatic nerve crush injury by RNA sequencing (RNA-Seq) and found that the hub gene Vav1 was highly expressed at both early response and regenerative stages of sciatic nerve injury. Furthermore, Vav1 was required for axon regeneration of dorsal root ganglia (DRG) neurons and functional recovery. Krüppel-like factor 2 (Klf2) was induced by retrograde Ca2+ signaling from injured axons and could directly promote Vav1 transcription in adult DRG neurons. The increased Vav1 then promoted axon regeneration by activating Rac1 GTPase independent of its tyrosine phosphorylation. Collectively, these findings break through previous limited cognition of Vav1, and first reveal a crucial role of Vav1 as a molecular switch in response to axonal injury for promoting axon regeneration, which might further serve as a novel molecular therapeutic target for clinical nerve injury repair.
Overall, this study highlights the crucial role of Vav1 in axon regeneration. More importantly, the overexpression of Vav1 may represent a novel molecular therapy for the treatment of peripheral nerve injury.
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