Abstract
Epithelial-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells is considered to be the main mechanism of proliferative vitreoretinopathy (PVR). Our previous study demonstrated that microRNA-29b (miR-29b) and its target protein kinase B (Akt2) played vital roles in this process. miR-29b, a mesenchymal marker α-smooth muscle actin (α-SMA) and the epithelial marker E-cadherin were assessed in epiretinal membranes of patients with PVR. The potential mechanism of miR-29b and EMT was also investigated. The expression levels of miR-29b, E-cadherin, and α-SMA in PVR epiretinal membranes were measured using quantitative PCR. The expression levels of Akt2, phosphorylated (p)-Akt2, p65, p-p65, and Snail in ARPE-19 cells were assessed using western blotting. The expression levels of miR-29b were positively correlated with E-cadherin mRNA expression, while an inverse correlation was observed between miR-29b and α-SMA mRNA expression in epiretinal membranes of patients with PVR. When miR-29b was transfected into ARPE-19 cells, the expression levels of Akt2, p-Akt2, p-p65 and Snail were downregulated. shRNA-Akt2 inhibited p-p65 and Snail expression, while the NF-κB inhibitor BAY11-7082 reduced Snail expression. The Akt2/p-p65/Snail pathway may be the underlying mechanism of miR-29b in EMT of RPE cells. The results of the present study may provide a new strategy for prevention and therapy of PVR.