Effect of autophagy modulators on vascular, glial and neuronal alterations in the oxygen-induced retinopathy mouse model

SUBIRADA, P. V.; PAZ, M.C.; RIDANO, ME; LORENC, V.E; FADER KAISER, C; CHIABRANDO, G. A.; SANCHEZ, M.C.

Frontiers in cellular neuroscience

Egidio D?Angelo, Christian Hansel,

Lugar: Lausanne; Año: 2019

1662-5102

ypoxia is one of the main insults in proliferative retinopathies, leading toneovascularization and neurodegeneration. To maintain homeostasis, neurons require efficient degradation and recycling systems. Autophagy participates in retinal cell death, but it is also a cell survival mechanism. Here, we analysed the role of autophagy at the three characteristic time periods in the oxygen-induced retinopathy (OIR) mouse model and determined if its modulation can improve vascular and non-vascular alterations.Experiments were performed with chloroquine (CQ) in order to monitor autophagosome accumulation by lysosomal blockade. Postnatal day (P)17 OIR mouse retinas showed a significant increase in autophagy flux. In particular, an intense LC3B and p62 staining was observed in inner layers of the retina, mainly proliferating endothelial cells. After a single intraocular injection of Rapamycin at P12 OIR, a decreased neovascular area and vascularendothelial growth factor (VEGF) protein expressio