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MicroRNA-182-5p Protects Human Lens Epithelial Cells Against Oxidative Stress-induced Apoptosis by Inhibiting NOX4 and P38 MAPK Signalling

Overview
Journal BMC Ophthalmol
Publisher Biomed Central
Specialty Ophthalmology
Date 2020 Jun 20
PMID 32552665
Citations 16
Authors
Affiliations
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Abstract

Background: MicroRNAs (miRNAs) are abnormally expressed in various ocular diseases, including age-related cataract. However, the role of miR-182-5p in the progression of age-related cataract remains unclear.

Methods: The expression of miR-182-5p in HLE-B3 cells was detected by qRT-PCR. HLE-B3 cells were transfected with miR-182-5p mimics. CCK-8, EdU, flow cytometry, 2',7'-dichlorodihydrofluorescein diacetate, JC-1 kit, and western blot were used to assess the cell viability, proliferation, apoptosis, reactive oxygen species (ROS) level, mitochondrial membrane potential (MMP), and protein expression, respectively, in vitro. The relationship between miR-182-5p and NOX4 was confirmed using the dual-luciferase reporter gene analysis.

Results: We found that miR-182-5p expression was significantly decreased by the HO exposure. Overexpression of miR-182-5p promoted cell proliferation and inhibited ROS production and apoptosis in HO-induced HLE-B3 cells. Moreover, p-p-38, p-ERK, and p-JNK were up-regulated in HO-treated HLE-B3 cells, and overexpression of miR-182-5p reversed the effects of HO on HLE-B3 cells. In addition, dual-luciferase reporter assay substantiated that NOX4 was a direct target and downregulated by miR-182-5p.

Conclusions: We concluded that miR-182-5p inhibited lens epithelial cells apoptosis through regulating NOX4 and p38 MAPK signaling, providing a novel biomarker for treatment of age-related cataract.

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References
1.
Xu Y, Zhang J, Fan L, He X . miR-423-5p suppresses high-glucose-induced podocyte injury by targeting Nox4. Biochem Biophys Res Commun. 2018; 505(2):339-345. DOI: 10.1016/j.bbrc.2018.09.067. View

2.
Huang Y, Cai G, Peng J, Shen C . Glucocorticoids induce apoptosis and matrix metalloproteinase-13 expression in chondrocytes through the NOX4/ROS/p38 MAPK pathway. J Steroid Biochem Mol Biol. 2018; 181:52-62. DOI: 10.1016/j.jsbmb.2018.03.001. View

3.
Bedard K, Krause K . The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology. Physiol Rev. 2007; 87(1):245-313. DOI: 10.1152/physrev.00044.2005. View

4.
Li Z, Deng W, Cao A, Zang Y, Wang Y, Wang H . Huangqi decoction inhibits hyperglycemia-induced podocyte apoptosis by down-regulated Nox4/p53/Bax signaling and . Am J Transl Res. 2019; 11(5):3195-3212. PMC: 6556627. View

5.
Asbell P, Dualan I, Mindel J, Brocks D, Ahmad M, Epstein S . Age-related cataract. Lancet. 2005; 365(9459):599-609. DOI: 10.1016/S0140-6736(05)17911-2. View