Abstract

A hyperglycemic environment can impair the function of keratinocytes, which is one of the key factors contributing to the difficulty in healing diabetic-related wounds. The abnormal expression of microRNAs (miRNAs) in the skin plays a significant role in wound healing. Therefore, the purpose of this study is to investigate the effects of miR-193a-3p on human keratinocytes (HaCaT) and its underlying mechanisms. The study established a HaCaT cell model treated with a high-glucose environment. The expression level of miR-193a-3p was assessed using quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability and migration were assessed using the Cell Counting Kit-8 (CCK-8) assay and Transwell experiments. Cell apoptosis was analyzed using flow cytometry. Inflammatory responses and oxidative stress were measured using enzyme-linked immunosorbent assay (ELISA) and corresponding kits. Additionally, the target of miR-193a-3p was verified using a dual-luciferase reporter assay. As a Result, High glucose (HG) treatment significantly upregulated the expression of miR-193a-3p, while inhibiting the proliferation and migration of HaCaT cells, promoting cell apoptosis, inflammatory responses, and oxidative damage. Inhibiting miR-193a-3p could reverse the inhibitory effect of HG on cell proliferation and migration, as well as its promoting effect on cell apoptosis. Mechanistically, miR-193a-3p participated in regulating cell proliferation, apoptosis, inflammation, and oxidative stress by targeting phosphatase and tensin homologue (PTEN). In conclusion, MiR-193a-3p regulates the proliferation, migration, apoptosis, inflammatory response, and oxidative stress of HaCaT cells by targeting PTEN.