Adiponectin inhibits high glucose-induced angiogenesis via inhibiting autophagy in RF/6A cells.

Adiponectin， one of the adipose-derived hormone with metabolic activity， has been reported to conversely affect angiogenesis of endothelial cells in vitro. The previous study in animal models has demonstrated that adiponectin has a protective role in retinal vascular injury following pathological stimuli. However， clinical research regarding the relationship between plasma adiponectin level and diabetic retinopathy (DR) are inconclusive. The aim of this study was to investigate the effect of adiponectin on high glucose-induced retinal angiogenesis and its association with autophagy by using rhesus choroid-retinal endothelial (RF-6A) cells as a model. We found that cell vitality decreased and cell migration and tube formation increased in the high-glucose group. Treatment with adiponectin or 3-methyladenine (3-MA， an autophagy inhibitor) increased cell viability and inhibited cell migration and tube formation. In the high-glucose group， the protein expression of Bax and apoptosis rate of cells increased and the expression of Bcl-2 decreased， whereas treatment with adiponectin or 3-MA reversed these results. Autophagy was activated in the high-glucose group to present as more LC3B fluorescent dots and higher expressions of LC3B， Atg5 proteins as well as lower expression of p62. Treatment with adiponectin or 3-MA inhibited autophagy by promoting the expression of p-PI3K， p-AKT， and p-mTOR when compared with the high-glucose group. The results of this study suggested that adiponectin inhibits high glucose-induced angiogenesis of RF/6A cells by inhibiting autophagy， and promotion of the PI3K/AKT/mTOR pathway might be involved in the anti-autophagy activities of adiponectin.