LINC00028 regulates the development of TGF beta 1-treated human tenon capsule fibroblasts by targeting miR-204-5p

Glaucoma is a leading cause of blindness worldwide with complex pathogenesis. The excessive proliferation and fibrosis of human tenon capsule fibroblasts (HTFs) trigger the scar formation after glaucoma filtration surgery. The purpose was to investigate the role of long intergenic non-protein coding RNA 28 (LINC00028) and mechanism in transforming growth factor beta 1 (TGF beta 1)-treated HTFs. The detection of LINC00028 and miR-204-5p expression was conducted using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was assessed by cell counting kit-8 (CCK-8) assay. Cell migration and invasion were monitored by transwell assay. The expression of Epithelial-mesenchymal transition (EMT)-related markers, including E-cadherin, alpha-Smooth muscle actin (alpha-SMA), fibronectin and beta-catenin, and autophagy-related markers, including Beclin 1 and light chain 3 (LC3-II and LC3-I) at the protein level was quantified using western blot. The prediction of the relationship between LINC00028 and miR-204-5p was performed by the online tool miRcode, and the verification of the relationship between them was conducted using dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay. The expression of LINC00028 was elevated in glaucoma tissues and TGF beta 1-treated HTFs. LINC00028 downregulation blocked proliferation, migration, invasion, EMT, fibrosis and autophagy of TGF beta 1-treated HTFs. MiR-204-5p was a target of LINC00028, and its reintroduction exerted a similar role of LINC00028 downregulation. The inhibition of miR-204-5p reversed the effects of LINC00028 downregulation in TGF beta 1-treated HTFs. LINC00028 regulated proliferation, migration, invasion, EMT, fibrosis and autophagy to induce the development of HTFs by competitively targeting miR-204-5p, and LINC00028 was regarded as a promising biomarker for glaucoma filtration treatment. (c) 2020 Elsevier Inc. All rights reserved.