Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 2.1
5-Year Impact Factor – 2.2
Scopus CiteScore – 3.4 (CiteScore Tracker 3.4)
Index Copernicus  – 161.11; MEiN – 140 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

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Advances in Clinical and Experimental Medicine

2018, vol. 27, nr 5, May, p. 577–582

doi: 10.17219/acem/69135

Publication type: original article

Language: English

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

Yuwen Wang1,A,D,F, Heding Zhou1,B,D,F, Xiaotian Liu1,C,D,F, Yin Han1,B,F, Suqi Pan1,B,F, Yanyan Wang1,C,F

1 Ningbo Eye Hospital, Ningbo, China

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.
Conclusion. 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.

Key words

cell apoptosis, H2O2, miR-181a, trabecular meshwork, nuclear factor-κB, c-Jun N-terminal kinase pathway

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