| Summary: | Abstract Background Dry eye disease (DED) is a ubiquitous and intricate ocular condition featured by the disruption of tear film homeostasis and inflammation of the ocular surface. This study aimed to examine the mechanism of interferon-inducible transmembrane protein 1 (IFITM1) in dry eye disease (DED). Methods HCE-T cells were damaged through exposure to hypertonic (NaCl) conditions. Cells with interferon-α (IFNα) knockdown and/or IFITM1 overexpression were established, and transfection efficiency was measured by reverse transcription‑quantitative PCR (RT‑qPCR). Flow cytometry was used to detect apoptosis. Western blot was exploited to measure apoptosis-related protein and IFITM1/extracellular signal-regulated kinase (ERK) pathway-related proteins to clarify the mechanism of IFITM1 inducing DED. Results The levels of IFNα in HCE-T cells were elevated under hypertonic conditions. Knockdown of IFNα suppressed the apoptosis, down-regulated the apoptosis proteins BCL2-Associated X (Bax), up-regulated B-cell lymphoma-2 (Bcl-2), diminished IFITM1 expression, and activated the ERK pathway. The overexpression of IFITM1 reversed the regulatory effects of IFNα knockdown on HCE-T cells. Conclusions Our research demonstrated that IFNα enhances IFITM1 to obstruct the ERK pathway and thus results in corneal epithelial cell injury. Knockdown of IFNα activates the ERK pathway via inhibiting IFITM1 to alleviate corneal epithelial cell damage. This study discovered the important role of the IFNα–IFITM1–ERK axis in DED and revealed the potential therapeutic targets for DED.
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