Plasma rich in growth factors reduces blue light‐induced oxidative damage on retinal pigment epithelial cells and restores their homeostasis by modulating vascular endothelial growth factor and pigment epithelium‐derived factor expression

活力测定 视网膜色素上皮 细胞生物学 超氧化物歧化酶 生长因子 氧化应激 血管内皮生长因子 PEDF公司 视网膜 血红素加氧酶 活性氧 细胞凋亡 内分泌学 癌症研究 血管内皮生长因子受体 生物 生物化学 血红素 受体
作者
Eduardo Anitua,María de la Fuente,Susana del Olmo‐Aguado,Carlota Suárez‐Barrio,Jesús Merayo‐Lloves,Francisco Muruzábal
出处
期刊:Clinical and Experimental Ophthalmology [Wiley]
卷期号:48 (6): 830-838 被引量:14
标识
DOI:10.1111/ceo.13767
摘要

Abstract Background This study analysed the effectiveness of plasma rich in growth factors (PRGF) in reducing the oxidative stress induced by blue light exposition on retinal pigment epithelial (RPE) cells. Methods Blood from six healthy donors was collected to obtain the PRGF. Retinal pigment epithelium (ARPE‐19) cells were exposed to blue light. Then, cells were incubated with PRGF or with control for 24 and 48 hours maintaining exposure to blue light. The cytoprotective effect of PRGF on ARPE cells was evaluated by measuring the cell viability, the reactive oxygen species (ROS) production and the expression of different proteins such as heme oxygenase 1 (HO‐1), catalase (CAT), superoxide dismutase (SOD‐1), apoptosis‐inducing factor (AIF), pigment epithelium‐derived factor (PEDF) and vascular endothelial growth factor (VEGF). Results The cell viability increased significantly at 24 and 48 hours after PRGF treatment compared to the control group. ROS synthesis was significantly reduced in PRGF‐treated cells with respect to control. Furthermore, the levels of HO‐1, SOD‐1 and AIF were significantly reduced after PRGF treatment at both times of treatment. However, CAT levels were only significantly reduced after PRGF treatment at 48 hours. The high expression of VEGF by RPE cells exposed to blue light was only counterbalanced in the PRGF group by increasing the expression of PEDF in comparison to the control group. Conclusion The present results show that PRGF treatment reduces the cytotoxic effects induced in RPE cells exposed to an oxidative stress environment. Furthermore, PRGF treatment preserves the mitochondrial activity and cell viability of RPE cells subjected to an oxidative stress.
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