Apelin supports primary rat retinal Muller cells under chemical hypoxia and glucose deprivation

Muller cells support the integrity of the blood-retinal barrier, whereas their dysfunction under pathological conditions may contribute to retinal edema formation. The apelin peptide, as the endogenous ligand of G protein-coupled receptor APJ, participates in numbers of physiological and pathological processes. Recent studies highlight its emerging role against ischemic injury. Our study aimed to investigate the potential neuroprotection of apelin for primary rat retinal Muller cells under hypoxia or glucose-deprivation (GD) by cell viability, migration and apoptosis, as well as apelin/APJ immunofluorescence labeling and mRNA expression. The results showed that exogenous apelin significantly stimulated Muller cells viability and migration under normal, hypoxic and glucose-free condition, also prevented apoptosis. Apelin immunoreactivities represented weak and diffuse staining in the cytoplasm, along with restricted nuclear APJ expression. They both appeared stronger immunoreactivities after 12 h hypoxia. Under hypoxic stress, apelin mRNA expression began to increase at 6 h (9.97 folds, p < 0.01), and APJ mRNA also up-regulated (2 h 6.50 folds, p < 0.05; 4 h 2.25 folds, p < 0.05; 6 h 14 folds, p < 0.01), whereas they both down-regulated during 4-12 h GD. Our results suggested that apelin induced the tolerance of Muller cells to hypoxia and GD. Its administration might be a promising protection for blood-retinal barrier to ischemia. (C) 2012 Elsevier Inc. All rights reserved.