miR-211 Regulates Cutaneous Wound Healing through Inhibiting Inflammatory Reactions and Oxidative Stress by Binding SOX11.

INTRODUCTION

Loss of skin integrity due to a wound or disease can lead to severe disability or even life threat. The highly expressed microRNAs in the skin are of great significance for skin development. The purpose of the investigation was to explore the effect and mechanism of miR-211 on inflammation, oxidative stress, and migration in keratinocytes.

METHODS

The HaCaT keratinocytes were treated with hydrogen peroxide (H2O2) to establish a wound-healing model. The expression of miR-211 was examined by quantitative real-time PCR. The cell function was reflected in proliferative ability, migration, apoptosis, and inflammation, which were evaluated using the Cell Counting Kit-8 (CCK-8) assay, transwell test, flow cytometry technique, and enzyme-linked immunosorbent assay (ELISA). The target of miR-211 was verified by luciferase luminescence measurements.

RESULTS

H2O2 inhibited HaCaT cell proliferation, migration, and promoted cell apoptosis, accompanied with the downregulation of miR-211. H2O2 led to inflammatory response and oxidative damage to HaCaT. miR-211 promoted proliferation and migration but improved cell apoptosis of HaCaT. The role of H2O2 on inflammatory response and oxidative stress was alleviated by miR-211. SRY-box transcription factor 11 (SOX11) was a targeted mediator of miR-211. SOX11 reversed the influence of miR-211 on cell proliferation, migration, apoptosis, inflammatory response, and oxidative stress.

CONCLUSION

miR-211 regulated the proliferation, migration, apoptosis, inflammation, and oxidative stress of keratinocytes by mediating SOX11, thus participating in cutaneous wound healing.