LncRNA MIAT increases cell viability, migration, EMT and ECM production in age-related cataracts by regulating the miR-181a/CTGF/ERK signaling pathway.

Abstract

Age-related cataract (ARC) is a common cause of blindness in elderly individuals. Long non-coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) has been reported to participate in various biological processes in a number of diseases; however, the biological mechanism underlying MIAT during ARC is not completely understood. The expression levels of MIAT, microRNA (miR)-181a and connective tissue growth factor (CTGF) were measured by reverse transcription-quantitative PCR. The protein expression levels of CTGF, α-smooth muscle actin, fibronectin, collagen type I, ERK, phosphorylated (p)-ERK, mitogen-activated protein kinase (MEK), and p-MEK were detected by western blotting. Cell viability and migration were assessed using MTT and Transwell assays, respectively. Moreover, a dual-luciferase reporter assay was performed to investigate the interaction between miR-181a and MIAT or CTGF. MIAT and CTGF were upregulated, while miR-181a was significantly downregulated in ARC tissues compared with normal tissues. MIAT or CTGF knockdown decreased cell viability, migration, epithelial-mesenchymal transition and extracellular matrix production in TGF-β2-treated SRA01/04 cells. It was hypothesized that miR-181a may be sponged by MIAT and may target CTGF. Furthermore, the miR-181a inhibitor reversed the inhibitory effect of MIAT knockdown on the progression of TGF-β2-treated SRA01/04 cells. Moreover, CTGF knockdown also reversed MIAT overexpression-mediated progression of TGF-β2-treated SRA01/04 cells. In addition, MIAT and CTGF regulated the activity of the ERK signaling pathway. The results suggested that MIAT may regulate the progression of ARC via the miR-181a/CTGF/ERK signaling pathway, which may serve as a novel therapeutic target for ARC.