In recent years, the potential involvement of numerous microRNAs (miRNAs) in glaucoma has been widely reported. However, the role of microRNA‑29b‑3p (miR‑29b‑3p) in the pathogenesis of glaucoma remains unknown. This study aimed to explore the biological role and regulatory mechanism of miR‑29b‑3p in the oxidative injury of human trabecular meshwork (HTM) cells induced by H2O2 stimulation. By establishing a glaucoma rat model, the effects of miR‑29‑3p in glaucoma were detected in vivo. Our findings demonstrated that miR‑29b‑3p was upregulated in a glaucoma model and antagomiR‑29b‑3p alleviated the symptoms of glaucoma. In vitro assays revealed that miR‑29b‑3p expression was significantly upregulated in HTM cells with H2O2 stimulation. Knockdown of miR‑29b‑3p alleviated H2O2 ‑induced oxidative injury in HTM cells by promoting cell viability, and inhibiting cell apoptosis, reactive oxygen species generation and extracellular matrix production. Subsequently, it was found that E3 ubiquitin‑protein ligase RNF138 (RNF138) was a downstream target of miR‑29b‑3p. RNF138 expression was downregulated in HTM cells with H2O2 stimulation. RNF138 knockdown significantly rescued the protective effect of miR‑29b‑3p inhibitor on HTM cells under oxidative injury. Additionally, miR‑29b‑3p silencing activated the ERK pathway via upregulating RNF138. Collectively, silencing of miR‑29b‑3p protected HTM cells against oxidative injury by upregulation of RNF138 to activate the ERK pathway.
Keywords: E3 ubiquitin‑protein ligase RNF138; ERK pathway; glaucoma; microRNA‑29b‑3p; oxidative stress.