作者: Fan Yang , Yujing Bai , Yanrong Jiang
DOI: 10.1016/J.PEPTIDES.2015.04.025
关键词: Vascular endothelial growth factor A 、 CCL2 、 Inflammation 、 Chemokine 、 Monocyte 、 Tumor necrosis factor alpha 、 Macrophage inflammatory protein 、 Chemistry 、 Endocrinology 、 Apelin 、 Internal medicine
摘要: Macrophages are an important source of pro-inflammatory and pro-angiogenic factors, which can promote pathological processes involving inflammation angiogenesis. This study investigated the effects Apelin on macrophages under both normal hypoxic conditions. Under culture conditions, down-regulated mRNA expression levels monocyte chemotactic protein 1 (MCP1), 3 (MCP3), macrophage inflammatory (MIP1α, MIP1β), vascular endothelial growth factor A (VEGFA), Angiopoietin 2 (Ang2) tumor necrosis α (TNFα). The supernatant concentrations MCP1, MCP3, MIP1α, MIP1β, (MIP2) TNFα proteins were significantly decreased in treated group. Hypoxia induced profound up-regulations angiogenic, chemokine, factors at levels. suppressed hypoxia-induced increases MIP2, MIP1β expression. underlying mechanism inhibit is regulating NF-κB/JNK signal pathway. Additionally, protect from apoptosis enhance cell migration during hypoxia. And cleaved Caspase9/3 pathways involved inhibiting RAW264.7 apoptosis. In conclusion, we showed effect condition, could further influence angiogenesis process that promoted by macrophages.