Downregulation of miR-20b-5p facilitates Mycobacterium tuberculosis survival in RAW 264.7 macrophages via attenuating the cell apoptosis by Mcl-1 upregulation.

摘要: Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis (Mtb). The interaction between Mtb and macrophages, which regulated microRNAs, determines the development of TB. However, function microRNA-20b-5p (miR-20b-5p) in RAW 264.7 macrophages against remains unknown. In this study, we analyzed expression level miR-20b-5p macrophage responses to infection exosomes derived from after infection. MiR-20b-5p mimics inhibitor were, respectively, transfected evaluate effect on macrophages. addition, targets were predicted a bioinformatics analysis. respectively with determine messenger RNA levels reverse transcription-polymerase chain reaction assay. results revealed that was decreased infected at different times. shown released Mtb. Upregulation suppressed survival while downregulation enhanced Overexpression cell viability induced apoptosis Mtb-infected underexpression increased vitality attenuated analysis Mcl-1 target miR-20b-5p. negatively Mcl-1. Overall, study first demonstrate present as potential therapeutic