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Retinoic acid regulates Schwann cell migration via NEDD9 induction by transcriptional and post-translational mechanisms.

Authors
  • Latasa, Maria-Jesus1
  • Jiménez-Lara, Ana María1
  • Cosgaya, Jose Miguel2
  • 1 Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid, Spain; Department of Endocrine and Nervous System Physiopathology, Arturo Duperier, 4, 28029 Madrid, Spain. , (Spain)
  • 2 Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid, Spain; Department of Endocrine and Nervous System Physiopathology, Arturo Duperier, 4, 28029 Madrid, Spain. Electronic address: [email protected] , (Spain)
Type
Published Article
Journal
Biochimica et Biophysica Acta
Publisher
Elsevier
Publication Date
Jul 01, 2016
Volume
1863
Issue
7 Pt A
Pages
1510–1518
Identifiers
DOI: 10.1016/j.bbamcr.2016.04.009
PMID: 27085739
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Schwann cell migration is essential during the regenerative response to nerve injury, however, the factors that regulate this phenomenon are not yet clear. Here we describe that retinoic acid (RA), whose production and signaling activity are greatly enhanced during nerve regeneration, increases Schwann cell migration. This is accompanied by the up-regulation of NEDD9, a member of the CAS family of scaffold proteins previously implicated in migratory and invasive behavior in gliomas, melanomas and the neural crest cells from which Schwann cells derive. This RA-induced NEDD9 accumulation is due to augmented mRNA levels, as well as an increase of NEDD9 protein stability. Although all NEDD9 phospho-isoforms present in Schwann cells are induced by the retinoid, the hormone also changes its phosphorylation status, thus altering the ratio between the different isoforms. Silencing NEDD9 in Schwann cells had no effect on basal migratory ability, but completely abrogated RA-induced enhanced migration. Collectively, our results indicate that RA could be a major regulator of Schwann cell migration after nerve injury, thus offering a new insight into peripheral nerve repair. Copyright © 2016 Elsevier B.V. All rights reserved.

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