AT-rich interaction domain 5A facilitates axon regeneration through docking protein 6 in the peripheral nervous system.

Background: Peripheral nerves are easily damaged in accidental trauma due to their shallow location. Compared to the limited regeneration of the central nerve, the peripheral nerve has a certain regenerative ability after injury. However, this ability is not sufficient to achieve functional recovery. To increase the rate of regeneration after nerve injury, increasing regeneration-associated gene expression by transcription factors in neurons is necessary. Methods: Sciatic nerve crush animal models were generated in Sprague-Dawley rats. Bioinformatics analysis and quantitative real-time polymerase chain reaction were applied to detect gene expression; immunofluorescence staining and western blotting were applied to detect protein expression. The neurite outgrowth of cultured dorsal root ganglion (DRG) neurons was performed to evaluate axon regeneration Result: Arid5a has high activity in specific regenerating clusters and it accumulates specifically in the nucleus of DRG neurons after sciatic nerve injury. Upon Arid5a inhibition by small interfering RNA, the outgrowth of neurites Conclusions: These findings indicate that axonal injury induced nucleus accumulation of Arid5a in neurons. Through Dok6, Arid5a accelerates axon regeneration of DRG neurons both