Long Non-Coding RNA MALAT1 Mediates Transforming Growth Factor Beta1-Induced Epithelial-Mesenchymal Transition of Retinal Pigment Epithelial Cells

Purpose To study the role of long non-coding RNA (lncRNA) MALAT1 in transforming growth factor beta 1 (TGF-beta 1)-induced epithelial-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells. Methods ARPE-19 cells were cultured and exposed to TGF-beta 1. The EMT of APRE-19 cells is confirmed by morphological change, as well as the increased expression of alpha-smooth muscle actin (alpha SMA) and fibronectin, and the down-regulation of E-cadherin and Zona occludin-1( ZO-1) at both mRNA and protein levels. The expression of lncRNA MALAT1 in RPE cells were detected by quantitative real-time PCR. Knockdown of MALAT1 was achieved by transfecting a small interfering RNA (SiRNA). The effect of inhibition of MALAT1 on EMT, migration, proliferation, and TGF beta signalings were observed. MALAT1 expression was also detected in primary RPE cells incubated with proliferative vitreoretinopathy (PVR) vitreous samples. Results The expression of MALAT1 is significantly increased in RPE cells incubated with TGF beta 1. MALAT1 silencing attenuates TGF beta 1-induced EMT, migration, and proliferation of RPE cells, at least partially through activating Smad2/3 signaling. MALAT1 is also significantly increased in primary RPE cells incubated with PVR vitreous samples. Conclusion LncRNA MALAT1 is involved in TGF beta 1-induced EMT of human RPE cells and provides new understandings for the pathogenesis of PVR.