Human amnion epithelial cell-derived exosomal miR-25-3p enhances mucin expression in conjunctival goblet cells via downregulating BCL2L11.

This study aimed to investigate the role of miR-25-3p carried by human amnion epithelial cell (hAEC)-derived exosomes in regulating MUC5AC production and apoptosis in conjunctival goblet cells. hAEC-derived exosomes were isolated, characterized, and evaluated for their uptake by conjunctival goblet cells. qRT-PCR, flow cytometry, Western blotting, and ELISA were used to assess the effects of exosomes on MUC5AC expression and apoptosis, with a focus on the contribution of miR-25-3p. The interaction between miR-25-3p and its predicted target BCL2L11 was examined using dual-luciferase reporter assays. Conjunctival goblet cells efficiently internalized hAEC-derived exosomes. Exosome treatment increased MUC5AC expression (P < 0.01) and reduced apoptosis (P < 0.01). miR-25-3p was found to mediate these effects, at least in part, through targeting BCL2L11, thereby promoting MUC5AC production (P < 0.01) and decreasing apoptosis (P < 0.01). hAEC-derived exosomes, particularly those containing miR-25-3p, modulate mucin expression and apoptosis in conjunctival goblet cells. These findings provide mechanistic insight into how exosomal miRNAs may contribute to maintaining ocular surface homeostasis, suggesting a potential role for exosomal miR-25-3p in supporting ocular surface health.