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

SUBIRADA, PV; PAZ, MC; RIDANO, ME; LORENC, VE; FADER, C; CHIABRANDO, GA; SANCHEZ, MC

Frontiers in Cellular Neuroscience

Frontiers Media S.A.

Año: 2019 vol. 13

1662-5102

ypoxia is one of the main insults in proliferative retinopathies, leading to neovascularization 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 characteristics time periods in the oxygen-induced retinopathy (OIR) mouse model and determining if its modulation can improve vascular and non-vascular alterations. 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 proliferating endothelial cells, in neovascular tufts, and photoreceptors. After a single intraocular injection of Rapamycin at P12 OIR, a decreased neovascular area and vascular endothelial growth factor (VEGF) protein expression were observed at P17 OIR. In addition, whereas the increased expression of glial fibrillary acidic protei