Upregulated miR-1298-5p sparks inflammatory onset and orchestrates pediatric dry eye disease progression.

PURPOSE

Dry eye disease (DED) is a multifactorial chronic ocular surface disorder with increasing annual prevalence in the pediatric population. MicroRNAs serve as biomarkers, yet the mechanistic role of miR-1298-5p in pediatric DED remains unclear. This study aims to investigate the role of miR-1298-5p in PDED and provide new insights into its clinical treatment.

METHODS

The study enrolled 71 PDED and 68 healthy controls. Tear miR-1298-5p levels were quantified via RT-qPCR, while ELISA and HPLC measured inflammatory cytokines and serum vitamin A. Pearson correlation analysis evaluated associations between miR-1298-5p expression and inflammatory cytokines and vitamin A levels. Multivariate logistic regression identified independent risk factors for PDED. An in vitro LPS-stimulated PDED model was established in human corneal epithelial cells, followed by miR-1298-5p inhibition to assess apoptosis and inflammation.

RESULTS

Inflammatory factors, vitamin A levels, and outdoor activity time were significant risk factors for pediatric PDED. The level of miR-1298-5p in the tears of children with PDED is 1.5 times higher than that in the healthy control group (P < 0.001). It shows a strong positive correlation with IL-6 (r = 0.687), TNF-α (r = 0.604), and IL-1β (r = 0.610), and a negative correlation with vitamin A (r = -0.566). Multivariate analysis showed that miR-1298-5p was the strongest predictor of PDED (OR = 17.08, 95% CI 6.13-47.55). In vitro, miR-1298-5p inhibition reduced LPS-induced HCEC apoptosis and inhibited the secretion of IL-6, TNF-α, and IL-1β inflammatory factors.

CONCLUSION

miR-1298-5p emerges as a novel PDED biomarker, correlating with inflammation and vitamin A. It exacerbates corneal damage through apoptotic/inflammatory pathways, offering therapeutic targets and mechanistic insights.