MicroRNA-191-5p ameliorates amyloid-β1-40 -mediated retinal pigment epithelium cell injury by suppressing the NLRP3 inflammasome pathway.

Amyloid β (Aβ) is a crucial component of drusen, the hallmark of the early stage of age-related macular degeneration (AMD), and can cause retinal pigment epithelium (RPE) cell damage through activation of the inflammatory response. MicroRNAs play a critical role in inflammation. However, the mechanism underlying the effect of microRNAs on the NLRP3 inflammasome induced by Aβ remains poorly understood. In the present study, we demonstrated that Aβ1-40 -mediated RPE damage by inducing a decrease in endogenous miR-191-5p expression. This led to the upregulation of its target gene, C/EBPβ. C/EBPβ acts as a transcription factor for NLRP3, promotes its transcription, and upregulates the downstream inflammatory factors Caspase-1 and IL-1β. Correspondingly, overexpression of miR-191-5p alleviated RPE cell injury by suppressing inflammation. The present study elucidates a novel transcriptional regulatory mechanism of the NLRP3 inflammasome. Our findings suggest an anti-inflammatory effect of miR-191-5p in Aβ1-40 -induced RPE impairment, shedding light on novel preventive or therapeutic approaches for AMD-associated RPE impairment.