MyD88 as a target of microRNA-203 in regulation of lipopolysaccharide or Bacille Calmette-Guerin induced inflammatory response of macrophage RAW264.7 cells

• miR-203 was directly targeting the 3′ untranslated region (3′UTR) of MyD88 and down-regulating the expression of protein.
• Overexpression of miR-203 was correlated with repressions of MyD88, as well as NF-κB, TNF-α and IL-6.
• miR-203 may be an important regulator in macrophages against LPS or mycobacteria infection.

MicroRNAs (miRNAs) have been demonstrated to play a pivotal role in the regulation of target gene expression at the post-transcriptional level. In order to better understand the role of microRNA-203 (miR-203) in the immunological regulation, the function of miR-203 was explored in the macrophage RAW264.7 cells against lipopolysaccharide (LPS) or Bacille Calmette-Guerin (BCG) stimulation. The results evidenced that myeloid differentiation factor 88 (MyD88) was a novel target of miR-203, miR-203 was capable of directly targeting the 3′ untranslated region (3′UTR) of MyD88 and post-transcriptionally down-regulating the expression of protein. In addition, an overexpression of miR-203 in RAW264.7 cells was correlated with repressions of MyD88, as well as its downstream signaling of NF-κB (NF-κB1), TNF-α and IL-6. These results suggest that miR-203 may be an important regulator in macrophages against LPS or mycobacteria infection, which may through a mechanism of negatively regulating MyD88-dependent Toll-like receptors signaling pathway.