MicroRNA-29a regulates lipopolysaccharide (LPS)-induced inflammatory responses in murine macrophages through the Akt1/NF-κB pathway

Aid activation in macrophages enhances lipopolysaccharide (LPS)-induced inflammatory responses through upregulation of the NF-kappa B signal pathway. Aid phosphorylation via microRNA (miR) caused the downregulation of Akt1. Here, we evaluated the role of miR-29a in LPS-triggered inflammatory responses. LPS stimulation of primary macrophages and RAW264.7 cells gradually increased the levels of miR-29a and was dependent on the LPS concentration. Overexpression of miR-29a in macrophages enhanced the expression of proinflammatory cytoldnes including IL-1 beta and IL-6, but not TNF-alpha. Conversely, knockdown of miR-29a diminished cytokine expression. Bioinformatics analyses indicated that Aktl was a potential target of miR-29a through its interaction with the CDS region of Akt1. The miR-29a also enhanced LPS-induced NF-kappa B signaling through increased NF-kappa B transcriptional activity and phosphorylation of p65, and through binding to Akt1. Moreover, Aktl silencing promoted the LPS-induced expression of IL-1 beta and IL-6, and upregulated the NF-kappa B pathway. Taken together, our results suggested that miR-29a participates in the regulation of inflammatory responses in LPS-stimulated macrophages by promoting NF-kappa B activation through targeting Akt1.