Abstract
Glaucoma is the main reason for irreversible blindness, and pathological increased intraocular pressure is the leading risk factor for glaucoma. It is reported that trabecular meshwork cell injury is closely associated with the elevated intraocular pressure. The current study aimed to investigate the role of small nucleolar RNA host gene 3 (SNHG3) in human trabecular meshwork (HTM) cells under oxidative stress. A series of experiments including real-time quantitative polymerase chain reaction, subcellular fractionation assay, western blot analysis, cell counting kit-8 assay, RNA pull down, flow cytometry analysis, and RNA immunoprecipitation assay were used to explore the biological function and regulatory mechanism of SNHG3 in HTM cells under oxidative stress. First, we observed that H2 O2 induced SNHG3 upregulation in HTM cells. Then, we found that SNHG3 silencing alleviated H2 O2 -induced oxidative damage in HTM cells. Moreover, snail family transcriptional repressor 2 (SNAI2) knockdown alleviated the oxidative damage induced by H2 O2 in HTM cells. Mechanistically, SNHG3 bound with ELAV like RNA binding protein 2 (ELAVL2) to stabilize SNAI2. Finally, SNAI2 overexpression counteracted the effect of SNHG3 silencing on H2 O2 -treated HTM cells. In conclusion, our results demonstrated that SNHG3 cooperated with ELAVL2 to modulate cell apoptosis and extracellular matrix accumulation by stabilizing SNAI2 in HTM cells under oxidative stress.
Highlights
Glaucoma is characterized by atrophy and depression of optic papilla, visual field defect and visual acuity decline [1,2]
Our results demonstrated that SNHG3 cooperated with ELAVL2 to modulate cell apoptosis and extracellular matrix (ECM) accumulation by stabilizing SNAI2 in human trabecular meshwork (HTM) cells under oxidative stress
The levels of extracellular matrix (ECM) proteins Collagen I, Collagen III, Fibronectin, MMP3, and MMP9 were obviously increased by H2O2 in HTM cells (Fig. 1C)
Summary
Glaucoma is characterized by atrophy and depression of optic papilla, visual field defect and visual acuity decline [1,2]. Pathological elevation of intraocular pressure and inadequate blood supply of optic nerve are the main reasons for glaucoma [3,4]. Previous research has showed that trabecular meshwork (TM) cells exert crucial effect on aqueous humour circulation, and TM cell injury is closely related to the elevated intraocular pressure [5,6]. In primary open angle glaucoma, increased intraocular pressure results in deformation at the optic nerve head; especially, intraocular pressure elevation leads to the deformation at the lamina cribrosa region where extracellular matrix (ECM) molecules such as fibronectin and collagen tend to accumulate [7,8,9]. It is reported that trabecular meshwork cell injury is closely associated with the elevated intraocular pressure. The current study aimed to investigate the role of SNHG3 in human trabecular meshwork (HTM) cells under oxidative stress
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