Artemin-GFRα3 interactions partially contribute to acute inflammatory hypersensitivity.

Autor: Thornton P; MedImmune, Granta Park, Cambridge CB21 6GH, UK. thorntonp@medimmune.com, Hatcher JP, Robinson I, Sargent B, Franzén B, Martino G, Kitching L, Glover CP, Anderson D, Forsmo-Bruce H, Low CP, Cusdin F, Dosanjh B, Williams W, Steffen AC, Thompson S, Eklund M, Lloyd C, Chessell I, Hughes J
Jazyk: angličtina
Zdroj: Neuroscience letters [Neurosci Lett] 2013 Jun 17; Vol. 545, pp. 23-8. Date of Electronic Publication: 2013 Apr 19.
DOI: 10.1016/j.neulet.2013.04.007
Abstrakt: The expression of artemin (ARTN), a glial cell line-derived neurotrophic factor (GDNF) family ligand, increases in pre-clinical models of nociception and recent evidence suggests this growth factor may play a causative role in inflammatory pain mechanisms. The aim of this study was to demonstrate functional inhibition of ARTN with monoclonal antibodies and to determine whether ARTN neutralisation could reverse inflammatory pain in mice. We show that monoclonal antibodies with high affinity to ARTN, completely inhibit ARTN-induced Ret and ERK activation in a human neuroblastoma cell line, and block capsaicin-induced CGRP secretion from primary rat DRG cultures. In addition, administration of anti-ARTN antibodies to mice provides a transient, partial reversal (41%) of FCA-induced mechanical hypersensitivity. Anti-ARTN antibodies had no effect on hypersensitivity in response to partial nerve ligation in mice. These data suggest that ARTN-GFRα3 interactions partially mediate early stage nociceptive signalling following an inflammatory insult.
(Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)
Databáze: MEDLINE
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