ERK1/2 pathway is activated in degenerated Rpe65-deficient mice.

Détails

ID Serval
serval:BIB_6FC1C3C8157A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
ERK1/2 pathway is activated in degenerated Rpe65-deficient mice.
Périodique
Experimental Eye Research
Auteur(s)
Métrailler S., Emery M., Schorderet D.F., Cottet S., Roduit R.
ISSN
1096-0007 (Electronic)
ISSN-L
0014-4835
Statut éditorial
Publié
Date de publication
2013
Peer-reviewed
Oui
Volume
116C
Pages
86-95
Langue
anglais
Notes
Publication types: JOURNAL ARTICLE
Résumé
The MAPK family is composed of three majors kinases, JNK, p38 and ERK1/2, and is implicated in many degenerative processes, including retinal cell death. The purpose of our study was to evaluate the activation of ERK1/2 kinase, and its potential role in Müller cell gliosis, during photoreceptor cell death in Rpe65(-/-) mice. We assayed ERK1/2 mRNA and protein levels, and evaluated ERK1/2 phosphorylation involved in kinase activation, in 2, 4 and 6 month-old Rpe65(-/-) mice and in age-matched wild-type controls. No differences in ERK1/2 expression were detected between Rpe65(-/-) and wild-type mice, however, ERK1/2 phosphorylation was dramatically increased in the knock out mice at 4 and 6 months-of-age. Phosphorylated ERK1/2 co-localized with GFAP in the ganglion cell layer, and correlated with an increase in GFAP protein expression and retinal cell death. Accumulation of cFOS protein in the ganglion cell layer occurred concomitant with pERK1/2 activation. Müller cell proliferation was not observed. ERK1/2 activation did not occur in 2 month-old Rpe65(-/-) or in the Rpe65(-/-)/Gnat1(-/-) mice, in which no degeneration was evident. The observed activation ERK1/2 and GFAP, both markers of Müller cell gliosis, in the absence of Müller cell proliferation, is consistent with the activation of atypical gliosis occurring during the slow process of degeneration in Rpe65(-/-) mice. As Müller cell gliosis is activated in many neuronal and retinal degenerative diseases, further studies will be needed to determine whether atypical gliosis in Rpe65(-/-) mice contributes to, or protects against, the pathogenesis occurring in this model of Leber congenital amaurosis.
Pubmed
Web of science
Création de la notice
07/10/2013 10:23
Dernière modification de la notice
20/08/2019 14:28
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