MicroRNA‐191‐5p ameliorates amyloid‐β 1‐40 –mediated retinal pigment epithelium cell injury by suppressing the NLRP3 inflammasome pathway

Abstract 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 Aβ 1‐40 ‐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 Aβ 1‐40 ‐induced RPE impairment, shedding light on novel preventive or therapeutic approaches for AMD‐associated RPE impairment.