High‐concentration atropine induces corneal epithelial cell apoptosis via miR‐30c‐1/SOCS3

Abstract

Abstract Atropine is an anticholinergic drug widely used in the field of ophthalmology, but its abuse can cause cytotoxicity to the cornea, resulting in blurred vision. This study used cultured human corneal epithelial cells (HCECs) to investigate the mechanism of high‐concentration atropine‐induced cytotoxicity. HCECs were treated with different concentrations of atropine. The expression levels of microRNA (miR)‐30c‐1 and suppressor of cytokine signaling 3 (SOCS3) were manipulated in HCECs treated with 0.1% atropine. Cell counting kit‐8 assay and flow cytometry were used to assess the viability and apoptosis of HCECs. The relationship between miR‐30c‐1 and SOCS3 was obtained from an online database and validated using a dual‐luciferase reporter assay and RNA immunoprecipitation method. The effect of atropine on the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway was also investigated. High‐concentration atropine inhibited the viability of HCECs and promoted their apoptosis. Moreover, atropine reduced miR‐30c‐1 expression and increased SOCS3 expression in a dose‐dependent manner. It was found that miR‐30c‐1 targeted SOCS3. Overexpression of miR‐30c‐1‐reduced atropine‐induced HCEC cytotoxicity, whereas upregulation of SOCS3 reversed the effects of miR‐30c‐1 overexpression. High‐concentration atropine inhibited activation of the JAK2/STAT3 signaling pathway via miR‐30c‐1/SOCS3. High‐concentration atropine induces HCEC apoptosis by regulating the miR‐30c‐1/SOCS3 axis and JAK2/STAT3 signaling pathway.

Keywords

• atropine
• human corneal epithelial cell
• JAK2/STAT3
• miR‐30c‐1
• SOCS3