Gal-1 expression and glycosylation pattern of retinas in a murine model of oxygen-induced retinopathy

VALERIA E. LORENC; JOSE D. LUNA PINTO; PAULA SUBIRADA; DIEGO O. CROCI RUSSO; MARIA CECILIA SANCHEZ; MAGALI E. RIDANO; MARIA CONSTANZA PAZ; GABRIEL A. RABINOVICH

Villa General Belgrano - Córdoba

Congreso; GlycoAR 2016; 2016

Neovascular retinopathies are leading causes of irreversible blindness. Oxygen Induced Retinopaty (OIR) mouse model has been developed in order to study the angiogenic pathomechanisms generated by hypoxic stimulus in these human diseases. Galectin-1 (Gal-1) is a lectin with high affinity for β-galactoside sugars through its carbohydrate recognition domain (CRD). This binding has been directly implicated with neovascular process in tumors. Here, our aim was to analyze Gal-1 expression and glycosylation pattern of normal and neovascular mice retinas.C57BL/6 mice were exposed to 75% O2 from postnatal day 7 (P7) to P12, after that they were returned to room air (RA) for additional five (P17) or nine days (P26). Age-matched mice maintained in RA were used as controls. At P12, P17 and P26 mice were sacrificed. In retinas, Gal-1 expression levels were analyzed by western blot and real time PCR (qRT-PCR) assays. Gal-1 localization and glycosylation pattern of mice retinas were studied by immunofluorescence with antibodies against Gal-1 and staining with biotinylated LEL and SNA lectins.Gal-1 expression was significantly increased in P17 OIR coincident with the highest levels of VEGF and mainly localized in the inner layers of retina with a similar pattern of LEL reactivity. SNA reactivity predominated in ganglion cell layer and it was different to Gal-1 expression pattern.These results suggest that Gal-1 through its CRD domain may participate in ischemic neovascular retinopathies.