Tgfbi/Bigh3 silencing activates ERK in mouse retina. (November 2015)

• Record Type: Journal Article
• Authors: Allaman-Pillet, Nathalie; Oberson, Anne; Bustamante, Mauro; Tasinato, Andrea; Hummler, Edith; Schorderet, Daniel F.
• Is Part Of: Experimental eye research. Volume 140(2015:Nov.)
• Page Start: 159
• Page End: 170
• Publication Date: 2015-11
• Subjects: BIGH3/TGFBI -- Retina -- Cornea -- ERK -- Apoptosis; Ophthalmology -- Periodicals; Eye -- Periodicals; Œil -- Périodiques; Ophthalmology; Periodicals; Electronic journals; 612.8405
• DOI: 10.1016/j.exer.2015.09.004
• Languages: English
• ISSNs: 0014-4835

Abstract

Abstract: 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. Highlights: Bigh3 is expressed in the retinal pigment epithelium. Bigh3 silencing induces a transient decrease in the apoptotic process involved in mice retina maturation after birth. The ERK pathway is involved in the pro-survival response following Bigh3 silencing.