18
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      MicroRNA-9 regulates mammalian axon regeneration in peripheral nerve injury

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Effective axon regeneration is achieved mainly by precise regulation of gene expression after peripheral nerve injury. MicroRNAs play an important role in controlling axon regeneration owe to its key epigenetic function in regulating gene expression. Here, we reveal that microRNA-9 (miR-9) may be a new suppressor of axon regeneration and FoxP1 is the functional target of miR-9. High level of endogenous miR-9 in sensory neurons inhibited axon regeneration in vitro and in vivo. In addition, the regulatory effect of miR-9 was mediated by changes in FoxP1 levels. Full rescuing effect of axon regeneration was achieved by FoxP1 up-regulation. Most importantly, we showed that miR-9-FoxP1 might be a new signaling pathway to regulate mammalian axon regrowth. Moreover, we provided the first evidence that maintaining a higher level of FoxP1 in sensory neurons by the microRNA is necessary for efficient axon regeneration.

          Related collections

          Most cited references30

          • Record: found
          • Abstract: found
          • Article: not found

          microRNA-9 regulates axon extension and branching by targeting Map1b in mouse cortical neurons.

          The capacity of neurons to develop a long axon and multiple dendrites defines neuron connectivity in the CNS. The highly conserved microRNA-9 (miR-9) is expressed in both neuronal precursors and some post-mitotic neurons, and we detected miR-9 expression in the axons of primary cortical neurons. We found that miR-9 controlled axonal extension and branching by regulating the levels of Map1b, an important protein for microtubule stability. Following microfluidic separation of the axon and the soma, we found that miR-9 repressed Map1b translation and was a functional target for the BDNF-dependent control of axon extension and branching. We propose that miR-9 links regulatory signaling processes with dynamic translation mechanisms, controlling Map1b protein levels and axon development.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The emerging field of neuroepigenetics.

            J. Sweatt (2013)
            Over the past 25 years, the broad field of epigenetics and, over the past decade in particular, the emerging field of neuroepigenetics have begun to have tremendous impact in the areas of learned behavior, neurotoxicology, CNS development, cognition, addiction, and psychopathology. However, epigenetics is such a new field that in most of these areas the impact is more in the category of fascinating implications as opposed to established facts. In this brief commentary, I will attempt to address and delineate some of the open questions and areas of opportunity that discoveries in epigenetics are providing to the discipline of neuroscience. Copyright © 2013 Elsevier Inc. All rights reserved.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              PI3K-GSK3 signaling regulates mammalian axon regeneration by inducing the expression of Smad1

              In contrast to neurons in the central nervous system, mature neurons in the mammalian peripheral nervous system can regenerate axons after injury, in part, by enhancing intrinsic growth competence. However, the signalling pathways that enhance the growth potential and induce spontaneous axon regeneration remain poorly understood. Here we reveal that phosphatidylinositol 3-kinase (PI3K) signalling is activated in response to peripheral axotomy and that PI3K pathway is required for sensory axon regeneration. Moreover, we show that glycogen synthase kinase 3 (GSK3), rather than mammalian target of rapamycin, mediates PI3K-dependent augmentation of the growth potential in the peripheral nervous system. Furthermore, we show that PI3K-GSK3 signal is conveyed by the induction of a transcription factor Smad1 and that acute depletion of Smad1 in adult mice prevents axon regeneration in vivo. Together, these results suggest PI3K-GSK3-Smad1 signalling as a central module for promoting sensory axon regeneration in the mammalian nervous system.
                Bookmark

                Author and article information

                Journal
                Mol Pain
                Mol Pain
                MPX
                spmpx
                Molecular Pain
                SAGE Publications (Sage CA: Los Angeles, CA )
                1744-8069
                05 June 2017
                2017
                : 13
                : 1744806917711612
                Affiliations
                [1 ]Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, China
                [2 ]Department of Orthopedic Surgery, The First Affiliated Hospital of China Medical University, Shenyang, China
                [3 ]Department of Orthopedic Surgery, China-Japan Union Hospital of Jilin University, Changchun, China
                [4 ]Department of Pain Management, Shengjing Hospital of China Medical University, Shenyang, China
                Author notes
                [*]Peng Yao, Department of Pain Management, Shengjing Hospital of China Medical University, Shenyang 110004, China. Email: proyaopeng@ 123456163.com
                Article
                10.1177_1744806917711612
                10.1177/1744806917711612
                5464514
                28480796
                e137606d-16b3-4b67-b797-c5dd7823c0d9
                © The Author(s) 2017

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 11 February 2017
                : 9 April 2017
                : 24 April 2017
                Categories
                Research Article
                Custom metadata
                January-December 2017

                Molecular medicine
                microrna-9,axon regeneration,peripheral nerve injury,electroporation
                Molecular medicine
                microrna-9, axon regeneration, peripheral nerve injury, electroporation

                Comments

                Comment on this article