Abstract
The trabecular meshwork (TM) plays a critical role in the outflow of aqueous humor. In this study, we aimed to investigate the effect of miR-181a on H2O2-induced apoptosis in TM cells. Human primary explant-derived TM cells were cultured in fibroblast medium and then treated with different concentrations of H2O2 for 2 h. We used a series of methods to carry out the research, such as MTT assay, quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR), apoptosis assay, and western blot methodology. The apoptosis assay and qRT-PCR showed that H2O2-induced apoptosis and cell viability were suppressed in a dose-dependent manner in TM cells. After the TM cells were treated with H2O2, miR-181a expression was significantly lower. The overexpression of miR-181a enhanced TM cells' viability, while the knockdown of miR-181a inhibited viability of cells. The overexpression of miR-181a suppressed TM cell apoptosis, while the knockdown of miR-181a induced apoptosis. H2O2 activated the nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase (JNK) pathways and induced cell apoptosis, while the overexpression of miR-181a suppressed both pathways and decreased the rate of apoptosis. In conclusion, this study indicated that miR-181a could improve the survival rate of TM cells after H2O2 treatment by blocking the NF-κB and JNK signaling pathways. These findings might provide novel therapeutic opportunities in the treatment of glaucoma.
Highlights
Worldwide, glaucoma is the one of the leading causes of irreversible blindness.[1,2] There are 60 million people diagnosed with glaucoma, of whom 8.4 million have been blinded due to glaucoma.[2]
The apoptosis assay and quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) showed that H2O2-induced apoptosis and cell viability were suppressed in a dose-dependent manner in trabecular meshwork (TM) cells
After the TM cells were treated with H2O2, miR-181a expression was significantly lower
Summary
Glaucoma is the one of the leading causes of irreversible blindness.[1,2] There are 60 million people diagnosed with glaucoma, of whom 8.4 million have been blinded due to glaucoma.[2] One of the major risk factors associated with glaucoma includes elevated hydrostatic pressure or intraocular pressure (IOP) in the eyes.[3] Intraocular pressure depends on the rate of formation and drainage of the aqueous humor via the trabecular meshwork.[3] The trabecular meshwork (TM), consisting of TM cells and located at the intraocular anterior chamber angle, plays a critical role in the outflow of aqueous humor.[4] Decreased outflow of aqueous humor induces an elevation in IOP and leads to glaucoma.[3,4] This in turn leads to increased oxidative DNA damage in the TM of glaucoma patients. The oxidative stress induces the activation of the nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase (JNK) signaling pathways.[5] Trabecular meshwork cells play an important role in maintaining the extracellular matrix synthesis (ECM) and phagocytosis of the debris in outflow tissues which control the aqueous-outflow facility. The trabecular meshwork (TM) plays a critical role in the outflow of aqueous humor
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