LAUSR

OBJECTIVE Retinal ganglion cells (RGCs) play a key role in the pathogenesis and development of glaucoma. The present study aims to investigate the underlying mechanism of long non-coding RNA (lncRNA) GAS5 in glaucoma development through regulating the apoptosis of RGCs. METHODS Rat models of chronic glaucoma were successfully established by translimbal laser photocoagulation. Retinal tissues were collected to determine the density of RGCs via Toluidine blue staining. The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis. The involvement of EZH2 and ATP-binding cassette transporter A1 (ABCA1) was further identified. Cell apoptosis after laser treatment and transfection was assessed by flow cytometry. RESULTS We found abundant GAS5 expression and a reduction in RGC density in the retinal tissues of glaucoma rats. Silencing of GAS5 led to increased EZH2 expression and decreased ABCA1 expression in RGCs. In addition, up-regulation of EZH2 promoted trimethylation of lysine 27 on histone H3, therefore suppressing ABCA1 expression, eventually leading to the inhibition of RGC apoptosis. CONCLUSION These findings provide further understanding of the function of GAS5 in RGC apoptosis. We conclude that down-regulation of GAS5 could help relieve glaucoma symptoms. GAS5 is therefore a promising target for developing novel therapeutic approaches for treating patients with glaucoma.