MicroRNA‑93 is overexpressed and induces apoptosis in glaucoma trabecular meshwork cells.

Abstract

Glaucoma is an optic neuropathy and a major cause of blindness globally. Trabecular meshwork cells are important in maintaining aqueous humor flow, the dysfunction of which tends to induce glaucoma. As important regulators of gene expression, microRNAs may be crucial in regulating trabecular meshwork cells. The present study aimed to reveal the effect of microRNA‑93 (miR‑93) on glaucoma trabecular meshwork (GTM) cell apoptosis. The expression levels of miR‑93 were compared between human trabecular meshwork (HTM) cells and GTM cells. The expression of miR‑93 was inhibited and increased by transfecting the cells with a lentivirus containing its specific inhibitor sponge and expression vector to investigate changes in GTM cell viability and apoptosis. Alterations in the protein expression of nuclear factor erythroid 2‑like2 (NFE2L2) were also examined to elucidate the possible mechanism underlying the effects of miR‑93. The results showed a marked promotion in the expression of miR‑93 in the GTM cells, compared with the HTM cells (P<0.01). GTM cell viability was increased and its apoptosis was inhibited by transfection with the miR‑93 sponge (P<0.01 and P<0.001, respectively), whereas the overexpression of miR‑93 abrogated these effects (P<0.05 and P<0.0001, respectively). The expression of NFE2L2, a possible target of miR‑93, was promoted by transfection with the miR‑93 sponge (P<0.01) and was inhibited in the cells overexpressing miR‑93 (P<0.01). Therefore, miR‑93 was capable of inhibiting viability and inducing apoptosis of the GTM cells, which was achieved via the suppression of NFE2L2. These results elucidated the pro‑apoptotic effects of miR‑93 in GTM cells and its possible functional mechanism, providing potential therapeutic targets for the treatment of glaucoma.