MiR-217 inhibition relieves oxidative stress-induced melanocyte damage by targeting sirtuin 1

Abstract

Vitiligo is caused by the disappearance of melanocyte function in the skin, but the mechanism has not been fully elucidated. This study aimed to investigate the expression and role of miR-217 in dysfunctional human primary melanocytes caused by oxidative stress, so as to explore its potential role in vitiligo. Hydrogen peroxide (H₂O₂) was used to induce the oxidative damage of melanocytes. The levels of sirtuin 1 (SIRT1) and miR-217 were measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and or Western blot assay. TargetScan and dual luciferase reporter gene assay were used to confirm the relationship between SIRT1 and miR-217. Cell viability and cell apoptosis were analysed by 3-(4,5-dimethyl-2-thiazolyl)−2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry assay, respectively. Reactive oxygen species (ROS) production, superoxide dismutase (SOD) and catalase (CAT) activities were determined using specific assay kits. SIRT1 was down-regulated, while miR-217 was up-regulated in H₂O₂-induced human primary melanocytes. SIRT1 was a target gene of miR-217. Inhibition of miR-217 increased cell viability and inhibited cell apoptosis in H₂O₂-treated melanocytes. Besides, inhibition of miR-217 enhanced the antioxidant activity of SOD and CAT and reduced the accumulation of intracellular ROS. Notably, all these effects were reversed by SIRT1-siRNA. The data indicated that SIRT1 was down-regulated, while miR-217 was up-regulated in dysfunctional human primary melanocytes caused by oxidative stress, and miR-217 inhibition relieved oxidative stress-induced melanocyte damage via targeting SIRT1, indicating that miR-217 might a potential target for vitiligo treatment.

Keywords:

• Oxidative stress
• melanocytes
• miR-217
• SIRT1
• vitiligo

Disclosure statement

Authors declare no conflict of interest.

Additional information

Funding

The present study was supported by the National Natural Science Foundation of China (grant no. 81773335, 81803131 and 81602755), Zhejiang Provincial Natural Science Foundation (grant no. LY18H110001) and Zhejiang Basic Public Welfare Research Project (grant no. LGF18H110002).