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MicroRNAs are emerging to be important epigenetic factors that control axon regeneration. Here, we report that microRNA-26a (miR-26a) is a physiological regulator of mammalian axon regeneration  in vivo . We demonstrated that endogenous miR-26a acted to target specifically glycogen synthase kinase 3 β  (GSK3 β ) in adult mouse sensory neurons  in vitro  and  in vivo . Inhibition of endogenous miR-26a in sensory neurons impaired axon regeneration  in vitro  and  in vivo . Moreover, the regulatory effect of miR-26a was mediated by increased expression of GSK3 β  because downregulation or pharmacological inhibition of GSK3 β  fully rescued axon regeneration. Our results also suggested that the miR-26a-GSK3 β  pathway regulated axon regeneration at the neuronal soma by controlling gene expression. We provided biochemical and functional evidences that the regeneration-associated transcription factor Smad1 acted downstream of miR-26a and GSK3 β  to control sensory axon regeneration. Our study reveals a novel miR-26a-GSK3 β -Smad1 signaling pathway in the regulation of mammalian axon regeneration. Moreover, we provide the first evidence that, in addition to inhibition of GSK3 β  kinase activity, maintaining a lower protein level of GSK3 β  in neurons by the microRNA is necessary for efficient axon regeneration.

MicroRNA-26a supports mammalian axon regeneration in vivo by suppressing GSK3β expression