Liu Mian, Gong Yi, Wei Jin-Yan, Xie Duo, Wang Jing, Yu Yan-Hong, Quan Song
Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.E-mail:
Nan Fang Yi Ke Da Xue Xue Bao. 2016 Jun 20;36(7):936-40.
To investigate the effect of prostaglandins E2 (PGE2) in enhancing vascular endothelial growth factor (VEGF) expression in a rat macrophage cell line and the effect of the media from PGE2-inuced rat macrophages on angiogenetic ability of human umbilical vein endothelial cells (HUVECs) in vitro.
Western blotting and qPCR were employed to investigate the expressions of VEGF protein and mRNAs in rat macrophage cell line NR8383 stimulated by PGE2 in the presence or absence of EP2 receptor inhibitor (AH6809) and EP4 receptor inhibitor (AH23848). Conditioned supernatants were obtained from different NR8383 subsets to stimulate HUVECs, and the tube formation ability and migration of the HUVECs were assessed with Transwell assay.
PGE2 stimulation significantly enhanced the expression of VEGF protein and mRNAs in NR8383 cells in a dose-dependent manner. The supernatants from NR8383 cells stimulated by PGE2 significantly enhanced tube formation ability of HUVECs (P<0.05) and promoted the cell migration. Such effects of PGE2 were blocked by the application of AH6809 and AH23848.
PGE2 can dose-dependently increase VEGF expression in NR8383 cells, and the supernatants derived from PGE2-stimulated NR8383 cells can induce HUVEC migration and accelerate the growth of tube like structures. PGE2 are essential to corpus luteum formation by stimulating macrophages to induce angiogenesis through EP2/EP4.
研究前列腺素E2(PGE2)增强大鼠巨噬细胞系中血管内皮生长因子(VEGF)表达的作用,以及PGE2诱导的大鼠巨噬细胞培养基对人脐静脉内皮细胞(HUVECs)体外血管生成能力的影响。
采用蛋白质免疫印迹法和定量聚合酶链反应(qPCR)研究在存在或不存在EP2受体抑制剂(AH6809)和EP4受体抑制剂(AH23848)的情况下,PGE2刺激大鼠巨噬细胞系NR8383中VEGF蛋白和mRNA的表达。从不同的NR8383亚群中获得条件上清液以刺激HUVECs,并通过Transwell实验评估HUVECs的管形成能力和迁移能力。
PGE2刺激以剂量依赖的方式显著增强了NR8383细胞中VEGF蛋白和mRNA的表达。PGE2刺激的NR8383细胞的上清液显著增强了HUVECs的管形成能力(P<0.05)并促进了细胞迁移。AH6809和AH23848的应用阻断了PGE2的这种作用。
PGE2可以剂量依赖地增加NR8383细胞中VEGF的表达,并且PGE2刺激的NR8383细胞产生的上清液可以诱导HUVEC迁移并加速管状结构的生长。PGE2通过刺激巨噬细胞通过EP2/EP4诱导血管生成,对黄体形成至关重要。