SNHG3 cooperates with ELAVL2 to modulate cell apoptosis and extracellular matrix accumulation by stabilizing SNAI2 in human trabecular meshwork cells under oxidative stress

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 H 2 O 2 induced SNHG3 upregulation in HTM cells. Then, we found that SNHG3 silencing alleviated H 2 O 2 -induced oxidative damage in HTM cells. Moreover, snail family transcriptional repressor 2 (SNAI2) knockdown alleviated the oxidative damage induced by H 2 O 2 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 H 2 O 2 -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.

Small Nucleolar RNAs in Pseudoexfoliation Glaucoma

“…SNHG3 silencing alleviated H 2 O 2 -induced oxidative damage in HTM cells. Moreover, SNHG3 cooperated with ELAV-like RNA-binding protein 2 (ELAVL2) to modulate cell apoptosis and ECM accumulation in HTM cells under oxidative stress [ 38 ]. Similar findings have been reported in another study using a model of H 2 O 2 -induced oxidative stress in HTM cells.…”

Dihydroartemisinin Attenuates Hypoxia-Induced Pulmonary Hypertension Through the ELAVL2/miR-503/PI3K/AKT Axis

“…Although ELAVL2 was originally identified as a neuron-specific protein, it has recently been found to function more widely in other tissues and cells. [26][27][28] In view of the low expression of ELAVL2 in mice treated under hypoxic conditions, we overexpressed it to explore its function (Fig. 6A, C).…”