Tgfbi/Bigh3 silencing activates ERK in mouse retina.

Détails

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Etat: Public
Version: Author's accepted manuscript
ID Serval
serval:BIB_D266D06B98BD
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Tgfbi/Bigh3 silencing activates ERK in mouse retina.
Périodique
Experimental Eye Research
Auteur(s)
Allaman-Pillet N., Oberson A., Bustamante M., Tasinato A., Hummler E., Schorderet D.F.
ISSN
1096-0007 (Electronic)
ISSN-L
0014-4835
Statut éditorial
Publié
Date de publication
2015
Peer-reviewed
Oui
Volume
140
Pages
159-170
Langue
anglais
Résumé
BIGH3 is a secreted protein, part of the extracellular matrix where it interacts with collagen and integrins on the cell surface. BIGH3 can play opposing roles in cancer, acting as either tumor suppressor or promoter, and its mutations lead to different forms of corneal dystrophy. Although many studies have been carried out, little is known about the physiological role of BIGH3. Using the cre-loxP system, we generated a mouse model with disruption of the Bigh3 genomic locus. Bigh3 silencing did not result in any apparent phenotype modifications, the mice remained viable and fertile. We were able to determine the presence of BIGH3 in the retinal pigment epithelium (RPE). In the absence of BIGH3, a transient decrease in the apoptotic process involved in retina maturation was observed, leading to a transient increase in the INL thickness at P15. This phenomenon was accompanied by an increased activity of the pro-survival ERK pathway.
Pubmed
Web of science
Open Access
Oui
Création de la notice
05/10/2015 10:27
Dernière modification de la notice
20/08/2019 15:52
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