MiR-205-3p protects human corneal epithelial cells from ultraviolet damage by inhibiting autophagy via targeting TLR4/NF-κB signaling

• Published in: European review for medical and pharmacological sciences Vol. 24; no. 12; p. 6494
• Main Authors: Fu, J-Y, Yu, X-F, Wang, H-Q, Lan, J-W, Shao, W-Q, Huo, Y-N
• Format: Journal Article
• Language: English
• Published: Italy 01.06.2020
• Subjects: Autophagy - physiology; Autophagy - radiation effects; Cell Line; Cell Survival - physiology; Cell Survival - radiation effects; Cornea - metabolism; Cornea - pathology; Cornea - radiation effects; Epithelial Cells - metabolism; Epithelial Cells - pathology; Epithelial Cells - radiation effects; Humans; MicroRNAs - biosynthesis; NF-kappa B - antagonists & inhibitors; NF-kappa B - biosynthesis; Signal Transduction - physiology; Signal Transduction - radiation effects; Toll-Like Receptor 4 - antagonists & inhibitors; Toll-Like Receptor 4 - biosynthesis; Ultraviolet Rays - adverse effects
• ISSN: 2284-0729
• DOI: 10.26355/eurrev_202006_21632

MiRNA has been found to have therapeutic effect on corneal damage. This paper aimed to study the effect of miR-205-3p on corneal damage induced by ultraviolet (UV) radiation. HCE cells were exposed to UV light and transfected. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot were used to determine miRNA/mRNA and protein expression. CCK-8 assay, Edu incorporation experiment, and flow cytometry were used to separately measure cell activity, proliferation and apoptosis. LC3 puncta were researched by immunofluorescence experiment. TNF-α, IL-6 and IL-1β levels in cells were detected by enzyme-linked immunosorbent assay (ELISA) kit. MDA, SOD, and GSH-PX levels were measured using detection kits. Reactive oxygen species (ROS) level was reflected by detecting DCFH-DA density. Luciferase activity assay was performed to verify the regulating relationship between miR-205-3p and TLR4. UV radiation decreased HCE cell viability, proliferation, and increased HCE cell apoptosis and autophagy (all p < 0.01). When exposed UV radiation, the overexpression of miR-205-3p group elevated HCE cells viability, proliferation and weakened HCE cells apoptosis and autophagy (all p < 0.01). MiR-205-3p inhibited inflammation and oxidative stress in HCE cells induced by UV radiation (p < 0.01). MiR-205-3p directly inhibited TLR4 expression. The upregulation of TLR4 significantly reversed the effects of miR-205-3p on HCE cells phenotypes induced by UV radiation (p < 0.01). MiR-205-3p protected HCE cells from UV damage by inhibiting autophagy via targeting TLR4.