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Autophagy induced by a novel triazol derivative promotes angiogenesis via decreasing interferon-inducible protein 10 level in vascular endothelial cells.

ABSTRACT
Autophagy plays an important role in angiogenesis, while the mechanisms of vascular endothelial cell (VEC) autophagy associated with angiogenesis remain unclear. In this study, we identified a novel triazol derivative (JL025) that significantly promoted angiogenesis both in vitro and in vivo. Moreover, JL025 had no effects on cell proliferation but dramatically increased the autophagy level of VEC. The suppression of autophagy inhibited JL025-induced angiogenesis in vitro and in vivo, suggesting that JL025-induced angiogenesis was dependent on the enhanced autophagy. Mechanistic studies indicated that JL025-induced VEC autophagy was related to the Akt/mTOR signaling pathway. Meanwhile, JL025 decreased the anti-angiogenic chemokine interferon-inducible protein 10 (IP10) protein level in HUVECs. Importantly, suppression of autophagy inhibited JL025-induced decrease of IP10 protein level, indicating that autophagy mediated the degradation of IP10. Taken together, our findings provide new insights into the relationship of VEC autophagy with angiogenesis, and JL025 may have a therapeutic potential in related diseases.