MiR-126 facilitates apoptosis of retinal ganglion cells in glaucoma rats via VEGF-Notch signaling pathway.

Abstract

The aim of this study was to explore the effect of micro ribonucleic acid (miR)-126 on the apoptosis of retinal ganglion cells in glaucoma rats via the vascular endothelial growth factor (VEGF)-Notch signaling pathway. A total of 36 Sprague-Dawley (SD) rats were randomly divided into three groups, including normal group (n=12), model group (n=12) and miR-126 antagomir group (n=12). Rats in normal group did not receive any treatment. In model group and miR-126 antagomir group, the rats were used to establish glaucoma models and intervened with normal saline and miR-126 antagomir, respectively. Intraocular pressure was detected at the completion of modeling and the last intervention, at 7 days after which samples were taken. Western blotting was adopted to detect the relative protein expressions of Notch1 and Notch2. The content of VEGF was examined via enzyme-linked immunosorbent assay (ELISA). Quantitative polymerase chain reaction (qPCR) was carried out to detect the messenger RNA (mRNA) expressions of VEGF, Notch1 and Notch2. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was performed to detect cell apoptosis. After modeling, intraocular pressure in model group and miR-126 antagomir group was significantly higher than that in normal group (p<0.05). At the end of the intervention, intraocular pressure in miR-126 antagomir group was notably lower than that in model group (p<0.05). VEGF content in model group and miR-126 antagomir group was notably higher than that in normal group (p<0.05). However, it was markedly lower in miR-126 antagomir group than model group (p<0.05). Model group exhibited remarkably higher protein expressions of Notch1 and Notch2 than normal group (p<0.05). However, the protein expressions of Notch1 and Notch2 in miR-126 antagomir group were evidently reduced (p<0.05). Besides, the mRNA expressions of VEGF, Notch1 and Notch2 in model group were significantly higher than those in normal group (p<0.05). However, they were significantly lower in miR-126 antagomir group than those in model group (p<0.05). Furthermore, the apoptosis rate in model group was distinctly higher than that in normal group (p<0.05). However, it was notably lower in miR-126 antagomir group than model group (p<0.05). MiR-126 facilitates the apoptosis of retinal ganglion cells in glaucoma rats by promoting the VEGF-Notch signaling pathway.