Pericytes are a population of cells that participate in normal vessel 
architecture and regulate permeability. Apelin, as the endogenous ligand of G 
protein-coupled receptor APJ, participates in a number of physiological and 
pathological processes. To date, the effect of apelin on pericyte is not clear. 
Our study aimed to investigate the potential protection mechanisms of apelin, 
with regard to primary rat retinal pericytes under hypoxia. Immunofluorescence 
staining revealed that pericytes colocalized with APJ in the fibrovascular 
membranes dissected from proliferative diabetic retinopathy patients. In the in 
vitro studies, we first demonstrated that the expression of apelin/APJ was 
upregulated in pericytes under hypoxia, and apelin increased pericytes 
proliferation and migration. Moreover, knockdown of apelin in pericyte was 
achieved via lentivirus-mediated RNA interference. After the inhibition of 
apelin, pericytes proliferation was inhibited significantly in hypoxia culture 
condition. Furthermore, exogenous recombinant apelin effectively prevented 
hypoxia-induced apoptosis through downregulating active-caspase 3 expression and 
increasing the ratio of B cell lymphoma-2 (Bcl-2)/Bcl-2 associated X protein 
(Bax) in pericytes. These results suggest that apelin suppressed hypoxia-induced 
pericytes injury, which indicated that apelin could be a potential therapeutic 
target for retinal angiogenic diseases.