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Effects of Lipoxin A4 on CoCl2-Induced Angiogenesis and Its Possible Mechanisms in Human Umbilical Vein Endothelial Cells

Lipoxin A4 (LXA4), a ‘stop signal’ for inflammation, is endogenously produced by eicosanoids, mainly via cell-to-cell interactions. At present, its influence on hypoxic angiogenesis, which is responsible for tumor growth and metastasis, has not been determined. Hypoxia regulates a variety of transcription factors including hypoxia-inducible factor (HIF)-1α, which plays a role in the expression of vascular endothelial growth factor (VEGF) and is considered a target for anti-angiogenic therapy. In this study, we utilized cobalt chloride (CoCl2) to mimic hypoxia in vitro. Data suggested that LXA4 decreased the expression and nucleus translocation of HIF-1α in a dose-dependent manner in CoCl2-treated human umbilical vein endothelial cells (HUVEC). Furthermore, we confirmed that LXA4 suppressed VEGF expression, tube formation and migration activity of HUVEC under hypoxia induced by CoCl2. These results suggest that LXA4 may have inhibitory effects on tumor angiogenesis through downregulation of the expression and nucleus translocation of HIF-1α. In summary, this study provides the first evidence for the anti-angiogenic role of LXA4 on hypoxic human endothelial cells, which may have therapeutic value for cancer and other angiogenesis-associated diseases.