miR-424-5p overexpression inhibits LPS-stimulated inflammatory response in bovine endometrial epithelial cells by targeting IRAK2.

Endometritis is inflammation of endometrium due to various factors and is a common cause of infertility. Several remedies used for endometritis like antibiotics, hormones, and herbs. Studies confirm that microRNAs play a significant role in various inflammatory diseases. However, the role of miR-424-5p in endometritis is not clear. In our study, histopathology, real-time quantitative polymerase chain reaction, Western blot analysis, immunofluorescence, ELISA, and dual-luciferase reporter assay were used to elucidate the effect of miR-424-5p in lipopolysaccharide (LPS)-primed inflammatory response in bovine endometrial epithelial cells (BEECs) and clarify the potential mechanism. Our results revealed that miR-424-5p mimics noticeably decrease the production of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), while miR-424-5p inhibitors have inverse effects in BEECs. Moreover, overexpression of miR-424-5p on BEECs cells also suppressed NF-κB p65 activation. Afterwards, we verified that miR-424-5p inhibited Interleukin 1 Receptor Associated Kinase 2 (IRAK2) expression by binding to the 3'-UTR of IRAK2 mRNA. Further, co-transfection of miR-424-5p inhibitors and siRNA-IRAK2 revealed that negative regulation of miR-424-5p on LPS-induced inflammatory response in BEECs was mediated by IRAK2.Mutually, miR-424-5p pharmacologic stabilization represents an entirely unique medical aid for cow endometritis and other inflammation-related diseases.