CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Autophagy participation in a mouse model of Oxygen-induced retinopathy (OIR)
Autor/es:
SUBIRADA, P. V.; RIDANO, ME; PAZ, M.C.; FADER KAISER, C; CHIABRANDO, G. A.; SANCHEZ, M.C.
Lugar:
Córdoba
Reunión:
Jornada; Jornada Regional de la Asociación de Investigación en Visión y Oftalmología (AIVO); 2015
Institución organizadora:
Comité AIVO
Resumen:
Autophagy has been implicated in neurodevelopment and other physiological processes. However, it has also been involved in cell survival or death in some diseases. In retinopathy of prematurity (ROP), the hypoxic insult generates damage in organelles and misfolding of retinal proteins, which could be eliminated by autophagy. Herein, we analyze the role of autophagy in the OIR model, which closely resemble ROP and Diabetic Retinopathy. C57/BL6 mice exposed to 75% O2 from postnatal day (P) 7 to 12, were brought to room air (RA) for additional five (P17) or nine days (P26). Age-matched mice maintained in RA for 17 or 26 days, respectively, were used as control. All mice were injected intraocularly with 3-methyladenine (an autophagy inhibitor) or saline, into one eye of each mouse, at two different times: P12 and P17. All animals were sacrificed at P26. Retinal function and morphology, cell death (TUNEL) and inmunofluorescence staining for autophagy (LC3) showed that the injection at P12, resulted in the more profound damage in both conditions, even though structural and functional alterations were more severe in OIR mice. Western blot of neural retinas allowed us to corroborate changes in stress and detoxifying proteins, whereas lysates of Müller cells under hypoxic conditions showed increased autophagy flux. The results suggest that autophagy blockade is detrimental for retinal tissue.