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Effect of miR-200b on retinal endothelial cell function under high glucose environment

机译:高糖环境下miR-200b对视网膜内皮细胞功能的影响

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摘要

As one of the important complications of diabetes, diabetic retinopathy (DR) presented high incidence worldwide. Hyperglycemia is an important promoting factor for DR occurrence and development. It can damage retinal endothelial cell, resulting in retinal structure and function disorder. Studies have shown that miR-200b may involve in regulating DR occurrence and development, but its specific function and mechanism have not been elucidated. This study aimed to investigate miR-200b effect and mechanism on human retinal endothelial cells (hRECs) under high glucose environment. hRECs were cultured under high glucose or normal environment. Real time PCR was applied to detect miR-200b expression. MiR-200b was transfected to hRECs and MTT was used to detect its effect on hRECs proliferation under high glucose environment. Real time PCR and Western blot were performed to determine VEGF and TGFβ1 expression in the retina endothelial cells. MiR-200b expression decreased significantly under high glucose environment, whereas hRECs proliferated obviously. Compared with normal control, VEGF and TGFβ1 mRNA and protein expression increased markedly (P < 0.05). After miR-200b transfection, miR-200b expression increased, while VEGF and TGFβ1 mRNA and protein expression decreased obviously. Compared with high glucose group, hRECs proliferation was inhibited (P < 0.05). MiR-200b can regulate RECs growth and proliferation by changing VEGF and TGFβ1 expression to delay DR.
机译:作为糖尿病的重要并发症之一,糖尿病性视网膜病(DR)在世界范围内发病率很高。高血糖是DR发生和发展的重要促进因素。它会损害视网膜内皮细胞,导致视网膜结构和功能紊乱。研究表明,miR-200b可能参与调节DR的发生和发展,但其具体功能和机制尚未阐明。这项研究旨在探讨miR-200b在高糖环境下对人视网膜内皮细胞(hRECs)的作用及其机制。 hRECs在高葡萄糖或正常环境下培养。应用实时PCR检测miR-200b表达。将MiR-200b转染至hRECs,MTT用于检测其在高葡萄糖环境下对hRECs增殖的影响。进行实时PCR和Western印迹以确定视网膜内皮细胞中VEGF和TGFβ1的表达。在高葡萄糖环境下,MiR-200b表达显着下降,而hRECs明显增生。与正常对照组相比,VEGF,TGFβ1mRNA和蛋白表达明显增加(P <0.05)。 miR-200b转染后,miR-200b的表达增加,而VEGF和TGFβ1的mRNA和蛋白的表达明显减少。与高糖组相比,hRECs的增殖受到抑制(P <0.05)。 MiR-200b可以通过改变VEGF和TGFβ1的表达来延缓DR,从而调节RECs的生长和增殖。

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