Abstract:
Objective To investigate expressions of microRNA-126(miR-126) and vascular endothelial growth factor (VEGF) in the epiretinal membrane tissues of patients with proliferative diabetic retinopathy (PDR) and their clinical significance.
Methods A total of 65 patients with PDR who underwent elective vitrectomy were selected as study group, and 62 patients with idiopathic macular hole who underwent vitrectomy at the same time were selected as control group. Quantitative Real-time Polymerase Chain Reaction(qRT-PCR) was used to detect the expression levels of miR-126 and VEGF mRNA in the epiretinal membrane tissues of the two groups; western blotting assay was used to detect the expression level of VEGF protein; fasting blood glucose (FBG), triglyceride (TG) and glycosylated hemoglobin (HbA1c) levels were detected; Pearson correlation analysis was used to analyze the correlation between miR-126 and VEGF mRNA and their correlations with FGB, HbA1c and TG were analyzed; Logistic multiple regression analysis was used to analyze the influencing factors for the occurrence of PDR.
Results The expression level of miR-126 in the epiretinal membrane of patients in the study group was significantly lower than that in the control group, VEGF mRNA and protein expression levels in the study group were significantly higher than those in the control group (P < 0.05). The levels of FGB, TG and HbA1c in the study group were significantly higher than those in the control group (P < 0.05). There were negative correlations of miR-126 with VEGF mRNA, FGB, HbA1c and TG (P < 0.05), and VEGF mRNA was positively correlated with FGB, HbA1c and TG (P < 0.05). Logistic multiple regression analysis showed that both miR-126 and VEGF mRNA were independent influencing factors for PDR in patients.
Conclusion The expression of miR-126 is decreased in the epiretinal membrane tissues of PDR patients, while the expression of VEGF is significantly increased. Therefore, miR-126 may be involved in the development and progression of PDR through negative regulation of VEGF expression.