miR-26a promotes axon regeneration in the mammalian central nervous system by suppressing PTEN expression

• Published in: Acta biochimica et biophysica Sinica Vol. 53; no. 6; pp. 758 - 765
• Main Authors: Zhang, Jing, Ma, Yan-Xia, Zeng, Yu-Qiang, Zhang, Shuang-Feng, Teng, Zhao-Qian, Gao, Jun, Liu, Chang-Mei
• Format: Journal Article
• Language: English
• Published: UK Oxford University Press 01.06.2021
• Subjects: Original
• ISSN: 1672-9145; 1745-7270
• DOI: 10.1093/abbs/gmab044

The permanent disability after the central nervous system (CNS) injury is due to the weakened regeneration ability of the damaged axon, resulting in the loss of the rebuilding functional relationship with the original targets. One determinant of successful axon regeneration is the activation of intrinsic axon growth ability of injured neurons. MicroRNAs are important epigenetic factors controlling axon regeneration. Here, we demonstrated that the expression of miR-26a in hippocampal neurons is upregulated developmentally. Inhibitions of endogenous miR-26a suppressed the axon growth in hippocampal neurons, and overexpression of miR-26a promoted its axon growth. We also found that the overexpression of miR-26a in retinal ganglion cells also promoted retinal ganglion cells’ survival and optic nerve regeneration. Moreover, endogenous miR-26a promotes the hippocampal neuronal axon growth by suppressing phosphatase and tensin homolog deleted on chromosome ten (PTEN) expression. Thus, our results suggested that the miR-26a‒PTEN pathway regulates CNS axon growth. Collectively, the study not only reveals a new mechanism underlying mammalian axon regeneration but also expands the pool of potential targets that can be manipulated to enhance CNS axon regeneration.