作者: Bufu Tang , Xingchen Li , Yanling Ren , Jing Wang , Di Xu
DOI: 10.1016/J.YEXCR.2017.08.013
关键词: Phosphorylation 、 Macrophage 、 Lipopolysaccharide 、 NF-κB 、 Downregulation and upregulation 、 Biology 、 Protein kinase B 、 Gene silencing 、 Proinflammatory cytokine 、 Cancer research 、 Cell biology
摘要: Akt activation in macrophages enhances lipopolysaccharide (LPS)-induced inflammatory responses through upregulation of the NF-κB signal pathway. phosphorylation via microRNA (miR) caused downregulation Akt1. Here, we evaluated role miR-29a LPS-triggered responses. LPS stimulation primary and RAW264.7 cells gradually increased levels was dependent on concentration. Overexpression enhanced expression proinflammatory cytokines including IL-1β IL-6, but not TNF-α. Conversely, knockdown diminished cytokine expression. Bioinformatics analyses indicated that Akt1 a potential target its interaction with CDS region The also LPS-induced signaling transcriptional activity p65, binding to Moreover, silencing promoted upregulated Taken together, our results suggested participates regulation LPS-stimulated by promoting targeting