Fig. 6: MiR-92a elevated the expression of p110δ and promoted TiPs-induced inflammation by targeting KLF4.

A Potential microRNAs interacting with KLF4 were sorted out from online platform The Encyclopedia of RNA Interactomes (ENCORI) and microRNAs were categorized by Venn chart. B Expressions of potential microRNAs upon 8 h TiPs stimulation were detected by qPCR assay. C, D mRNA (C) and protein levels (D) of KLF4 were respectively examined upon the transfection of mimics-miR-92a (Pre-92a) or inhibitor-miR-92a (Anti-92a). E Potential binding region of miR-92a and 3′UTR of KLF4, and relative sequence of KLF4 with mutant 3′UTR. F Dual luciferase activity was detected after 48 h transfection of wild-type KLF4 3′UTR (KLF4 3′UTR-WT) or mutant-type KLF4 3′UTR (KLF4 3′UTR-MT) with mimics-miR-92a (Pre-92a) or mimics-NC (Pre-NC). G, H mRNA level (G) and protein levels (H) of p110δ were respectively examined upon the transfection of mimics-miR-92a (Pre-92a) with or without KLF4-overexpressed plasmids (KLF4⁺). I Total p65, total IκBα, phosphorylated p65, and phosphorylated IκBα were detected by WB assay to determine the activation of NF-κB signaling pathway upon 1 h TiPs stimulation in mimics-miR-92a (Pre-92a)-transfected macrophages or inhibitor-miR-92a (Anti-92a)-transfected macrophages. J Supernatant levels of TNFα and IL-6 from miR-92a-increased or miR-92a-inhibited macrophages were analysed by ELISA assay after 8 h TiPs stimulation. All data were concluded from at least three independent assays. Statistic data were displayed as mean ± SEM and were conducted unpaired t test analysis or one-way ANOVA analysis to determine significant difference. *p < 0.05, **p < 0.01, ***p < 0.001 compared with the negative group.