SCIENCE@home

MiR-181a inhibits human trabecular meshwork cell apoptosis induced by H₂O₂ through the suppression of NF-κB and JNK pathways.

Yuwen Wang,He Zhou,Xiaotian Liu,Yin Han,S. Pan,Yanyan Wang

Published 2018 in Advances in Clinical and Experimental Medicine

ABSTRACT

BACKGROUND The trabecular meshwork (TM) plays a critical role in the outflow of aqueous humor. OBJECTIVES In this study, we aimed to investigate the effect of miR-181a on H2O2-induced apoptosis in TM cells. MATERIAL AND METHODS 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. RESULTS 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. CONCLUSIONS 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.

PUBLICATION RECORD

CITATION MAP

EXTRACTION MAP

CLAIMS

  • No claims are published for this paper.

CONCEPTS

  • No concepts are published for this paper.

REFERENCES

  • No references are available for this paper.

Showing 0-0 of 0 references · Page 1 of 1

CITED BY

Showing 1-17 of 17 citing papers · Page 1 of 1