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      Promotion of Peripheral Nerve Regeneration by Stimulation of the Extracellular Signal‐Regulated Kinase (ERK) Pathway

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          ABSTRACT

          Peripherally projecting neurons undergo significant morphological changes during development and regeneration. This neuroplasticity is controlled by growth factors, which bind specific membrane bound kinase receptors that in turn activate two major intracellular signal transduction cascades. Besides the PI3 kinase/AKT pathway, activated extracellular signal‐regulated kinase (ERK) plays a key role in regulating the mode and speed of peripheral axon outgrowth in the adult stage. Cell culture studies and animal models revealed that ERK signaling is mainly involved in elongative axon growth in vitro and long‐distance nerve regeneration in vivo. Here, we review ERK dependent morphological plasticity in adult peripheral neurons and evaluate the therapeutic potential of interfering with regulators of ERK signaling to promote nerve regeneration. Anat Rec, 302:1261–1267, 2019. © 2019 Wiley Periodicals, Inc.

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          Regulation of neuronal survival by the serine-threonine protein kinase Akt.

          H. Dudek, S. R. Datta, T Franke … (1997)
          A signaling pathway was delineated by which insulin-like growth factor 1 (IGF-1) promotes the survival of cerebellar neurons. IGF-1 activation of phosphoinositide 3-kinase (PI3-K) triggered the activation of two protein kinases, the serine-threonine kinase Akt and the p70 ribosomal protein S6 kinase (p70(S6K)). Experiments with pharmacological inhibitors, as well as expression of wild-type and dominant-inhibitory forms of Akt, demonstrated that Akt but not p70(S6K) mediates PI3-K-dependent survival. These findings suggest that in the developing nervous system, Akt is a critical mediator of growth factor-induced neuronal survival.
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            Coordinating ERK/MAPK signalling through scaffolds and inhibitors.

            Walter Kolch (2005)
            The pathway from Ras through Raf and MEK (MAPK and ERK kinase) to ERK/MAPK (extracellular signal-regulated kinase/mitogen-activated protein kinase) regulates many fundamental cellular processes. Recently, a number of scaffolding proteins and endogenous inhibitors have been identified, and their important roles in regulating signalling through this pathway are now emerging. Some scaffolds augment the signal flux, but also mediate crosstalk with other pathways; certain adaptors target MEK-ERK/MAPK complexes to subcellular localizations; others provide regulated inhibition. Computational modelling indicates that, together, these modulators can determine the dynamic biological behaviour of the pathway.
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              Sprouty1 and Sprouty2 provide a control mechanism for the Ras/MAPK signalling pathway.

              Takayuki Yasunaga, Eisuke NISHIDA, Hiroshi Hanafusa … (2002)
              Sprouty (Spry) inhibits signalling by receptor tyrosine kinases; however, the molecular mechanism underlying this function has not been defined. Here we show that after stimulation by growth factors Spry1 and Spry2 translocate to the plasma membrane and become phosphorylated on a conserved tyrosine. Next, they bind to the adaptor protein Grb2 and inhibit the recruitment of the Grb2-Sos complex either to the fibroblast growth factor receptor (FGFR) docking adaptor protein FRS2 or to Shp2. Membrane translocation of Spry is necessary for its phosphorylation, which is essential for its inhibitor activity. A tyrosine-phosphorylated octapeptide derived from mouse Spry2 inhibits Grb2 from binding FRS2, Shp2 or mouse Spry2 in vitro and blocks activation of the extracellular-signal-regulated kinase (ERK) in cells stimulated by growth factor. A non-phosphorylated Spry mutant cannot bind Grb2 and acts as a dominant negative, inducing prolonged activation of ERK in response to FGF and promoting the FGF-induced outgrowth of neurites in PC12 cells. Our findings suggest that Spry functions in a negative feedback mechanism in which its inhibitor activity is controlled rapidly and reversibly by post-translational mechanisms.
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                Author and article information

                Contributors
                Lars Klimaschewski:
                ORCID: https://orcid.org/0000-0003-3211-0047
                lars.klimaschewski@i-med.ac.at
                Journal
                Journal ID (nlm-ta): Anat Rec (Hoboken)
                Journal ID (iso-abbrev): Anat Rec (Hoboken)
                Journal ID (doi): 10.1002/(ISSN)1932-8494
                Journal ID (publisher-id): AR
                Title: Anatomical Record (Hoboken, N.j. : 2007)
                Publisher: John Wiley & Sons, Inc. (Hoboken, USA )
                ISSN (Print): 1932-8486
                ISSN (Electronic): 1932-8494
                Publication date (Electronic): 22 April 2019
                Publication date (Print): August 2019
                Volume: 302
                Issue: 8 , Thematic Group: Advances in our understanding of the morphological response to injury in the peripheral nervous system ( doiID: 10.1002/ar.v302.8 )
                Pages: 1261-1267
                Affiliations
                [ 1 ] Department of Anatomy, Histology and Embryology, Division of Neuroanatomy Medical University Innsbruck Innsbruck Austria
                Author notes
                [*] [* ] Correspondence to: Department of Anatomy, Histology and Embryology, Division of Neuroanatomy, Medical University Innsbruck, Muellerstrasse 59, 6020 Innsbruck, Austria

                E‐mail: lars.klimaschewski@ 123456i-med.ac.at

                Author information
                https://orcid.org/0000-0003-3211-0047
                Article
                Publisher ID: AR24126
                DOI: 10.1002/ar.24126
                PMC ID: 6767477
                PubMed ID: 30951263
                SO-VID: f95ef085-52e2-46ac-9360-8a9642e242f6
                Copyright © © 2019 The Authors. The Anatomical Record published by Wiley Periodicals, Inc. on behalf of American Association of Anatomists.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 14 September 2018
                Date revision received : 06 December 2018
                Date accepted : 11 January 2019
                Page count
                Figures: 1, Tables: 0, Pages: 7, Words: 6639
                Funding
                Funded by: Austrian Science Fund
                Award ID: P 28909‐BBL
                Categories
                Subject: Full Length Thematic
                Subject: Thematic Papers
                Subject: Full Length Thematic
                Custom metadata
                source-schema-version-number 2.0
                component-id ar24126
                cover-date August 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.9 mode:remove_FC converted:30.09.2019

                ScienceOpen disciplines: Anatomy & Physiology
                Keywords: growth factor,rtk,neuronal survival,axon,sprouty
                Data availability:
                ScienceOpen disciplines: Anatomy & Physiology
                Keywords: growth factor, rtk, neuronal survival, axon, sprouty

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