Zhang Guang-Hong, Qin Rui, Zhang Shui-Hua, Zhu He
Department of Ophthalmology, The No.474 Hospital of Chinese People's Liberation Army, Urumchi, 830011, China,
Mol Biol Rep. 2014 Feb;41(2):779-85. doi: 10.1007/s11033-013-2917-4. Epub 2013 Dec 30.
Vascular endothelial growth factor B (VEGF-B) was reported to be angiogenic, and it was considered as a neuroprotective agent in mouse retinal ganglion cells following optic nerve crush. Thus, it was necessary to investigate whether VEGF-B contributes to the process of retinal and choroidal neovascularization. We aimed to investigate the effects of VEGF-B on proliferation and migration in EA.Hy926 cells. The proliferation of cells was analyzed by cell counting kit 8 assay, and the migration of cells was evaluated by a modified Boyden chamber assay. The levels of phospho-ERK1/2 (P-ERK1/2), ERK1/2, phospho-p38 and p38 were detected by western blotting. The results showed that VEGF-B induced proliferation and migration of EA.Hy926 cells (P < 0.01 and P < 0.05, respectively), and ERK1/2 and p38 phosphorylation were significantly activated. Our study suggested that VEGF-B was an angiogenesis factor in vitro and that ERK1/2 and p38-related signaling pathways were involved in these VEGF-B activities.
据报道,血管内皮生长因子B(VEGF-B)具有血管生成作用,并且在小鼠视神经挤压后,它被视为一种保护视网膜神经节细胞的神经保护剂。因此,有必要研究VEGF-B是否参与视网膜和脉络膜新生血管形成过程。我们旨在研究VEGF-B对EA.Hy926细胞增殖和迁移的影响。通过细胞计数试剂盒8检测法分析细胞增殖情况,通过改良的Boyden小室检测法评估细胞迁移情况。采用蛋白质免疫印迹法检测磷酸化ERK1/2(P-ERK1/2)、ERK1/2、磷酸化p38和p38的水平。结果表明,VEGF-B诱导EA.Hy926细胞增殖和迁移(分别为P < 0.01和P < 0.05),并且ERK1/2和p38磷酸化被显著激活。我们的研究表明,VEGF-B在体外是一种血管生成因子,并且ERK1/2和p38相关信号通路参与了这些VEGF-B的活性。