The SELENOT mimetic PSELT promotes nerve regeneration by increasing axonal myelination in a facial nerve injury model in female rats.
PSELT
RRID:AB_2144666
RRID:AB_2340376
RRID:AB_2340607
RRID:AB_2340812
RRID:AB_2811056
RRID:AB_95186
SELENOT
axotomy
facial nerve
motor unit
myelin
peptide
selenoprotein
therapy
Journal
Journal of neuroscience research
ISSN: 1097-4547
Titre abrégé: J Neurosci Res
Pays: United States
ID NLM: 7600111
Informations de publication
Date de publication:
09 2022
09 2022
Historique:
revised:
17
03
2022
received:
13
07
2021
accepted:
06
06
2022
pubmed:
23
6
2022
medline:
22
7
2022
entrez:
22
6
2022
Statut:
ppublish
Résumé
Peripheral nerve injury (PNI) is frequent and many patients suffer lifelong disabilities in severe cases. Although the peripheral nervous system is able to regenerate, its potential is limited. In this study, we tested in a nerve regeneration model in rat the potential beneficial effect of a short mimetic peptide, named PSELT, which derives from SELENOT, an essential thioredoxin-like selenoprotein endowed with neuroprotective and antioxidant activities. For this purpose, the right facial nerve of female Long-Evans rats was axotomized then bridged with a free femoral vein interposition graft. PSELT (1 μM) was injected into the vein immediately and 48 h after the injury, and the effects observed were compared to those found after an end-to-end suture used as a gold standard treatment. Whisking behavior, electrophysiological potential, and histological analyses were performed 3 months after injury to determine the effects of these treatments. These analyses revealed that PSELT-treated animals exhibit a better motor recovery in terms of protraction amplitude and velocity of vibrissae compared to control and end-sutured nerve animal groups. Moreover, administration of PSELT following injury enhanced muscle innervation, axonal elongation, and myelination of newly formed nerve fibers. Altogether, these results indicate that a PSELT-based treatment is sufficient to enhance facial nerve myelination and regeneration and could represent a new therapeutic tool to treat PNI.
Identifiants
pubmed: 35730417
doi: 10.1002/jnr.25098
pmc: PMC9545325
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1721-1731Informations de copyright
© 2022 The Authors. Journal of Neuroscience Research published by Wiley Periodicals LLC.
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