title: Effects of Apelin on RAW264.7 cells under both normal and hypoxic conditions.
abstract: Macrophages are an important source of pro-inflammatory and pro-angiogenic factors, which can promote pathological processes involving inflammation and angiogenesis. This study investigated the effects of Apelin on macrophages under both normal and hypoxic conditions. Under normal culture conditions, Apelin down-regulated the mRNA expression levels of monocyte chemotactic protein 1 (MCP1), monocyte chemotactic protein 3 (MCP3), macrophage inflammatory protein 1 (MIP1α, MIP1β), vascular endothelial growth factor A (VEGFA), Angiopoietin 2 (Ang2) and tumor necrosis factor α (TNFα). The supernatant concentrations of MCP1, MCP3, MIP1α, MIP1β, macrophage inflammatory protein 2 (MIP2) and TNFα proteins were significantly decreased in the Apelin treated group. Hypoxia induced profound up-regulations of the angiogenic, chemokine, and inflammatory factors at both the mRNA and protein levels. Apelin suppressed the hypoxia-induced increases in MCP1, MCP3, MIP2, MIP1β and TNFα expression. The underlying mechanism of Apelin inhibit inflammation is regulating NF-κB/JNK signal pathway. Additionally, Apelin can protect macrophages from apoptosis and can enhance cell migration during hypoxia. And cleaved Caspase9/3 pathways were involved in Apelin inhibiting RAW264.7 apoptosis. In conclusion, we showed the effect of Apelin on RAW264.7 macrophage under normal and hypoxic condition, which could further influence the angiogenesis and inflammation process that promoted by macrophages.
authors.affiliation: Department of Ophthalmology, Peking University People's Hospital, Key Laboratory of Vision Loss and Restoration, Ministry of Education, Beijing Key Laboratory for the Diagnosis and Treatment of Retinal and Choroid Diseases, Beijing, China.
authors.forename: Fan
authors.initials: F
authors.lastname: Yang
authors.affiliation: Department of Ophthalmology, Peking University People's Hospital, Key Laboratory of Vision Loss and Restoration, Ministry of Education, Beijing Key Laboratory for the Diagnosis and Treatment of Retinal and Choroid Diseases, Beijing, China. Electronic address: baiyujing93@gmail.com.
authors.forename: Yujing
authors.initials: Y
authors.lastname: Bai
authors.affiliation: Department of Ophthalmology, Peking University People's Hospital, Key Laboratory of Vision Loss and Restoration, Ministry of Education, Beijing Key Laboratory for the Diagnosis and Treatment of Retinal and Choroid Diseases, Beijing, China. Electronic address: drjiangyr@gmail.com.
authors.forename: Yanrong
authors.initials: Y
authors.lastname: Jiang
mesh_terms: D054392:Adipokines / Q000008:administration & dosage / Q000235:genetics / Q000378:metabolism*; D042702:Angiopoietin-2 / Q000096:biosynthesis; D000818:Animals; D000073861:Apelin; D002465:Cell Movement / Q000235:genetics; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics; D054407:Chemokine CCL4 / Q000096:biosynthesis / Q000235:genetics; D005786:Gene Expression Regulation / Q000187:drug effects; D007249:Inflammation / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D036341:Intercellular Signaling Peptides and Proteins / Q000008:administration & dosage / Q000235:genetics / Q000378:metabolism*; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D009389:Neovascularization, Pathologic / Q000235:genetics / Q000378:metabolism; D010455:Peptides / Q000008:administration & dosage / Q000138:chemical synthesis / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis
chemical_list: D054392:Adipokines; D042702:Angiopoietin-2; D000073861:Apelin; C402826:Apln protein, mouse; D018932:Chemokine CCL2; D054407:Chemokine CCL4; D036341:Intercellular Signaling Peptides and Proteins; D010455:Peptides; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse
keywords: Angiogenesis; Apelin; Hypoxia; Inflammation; Macrophage