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miRNA‐155 regulates the human inducible nitric oxide synthase gene expression

Recently, miRNA‐155 (miR‐155) has been identified as a component of the primary macrophage response to various inflammatory mediators such as TNF‐α, IFN‐β or LPS. These mediators can also strongly induce human iNOS (hiNOS) gene to produce high‐output hiNOS product, Nitric Oxide (NO). We hypothesized that miR‐155 might be capable of regulating the hiNOS gene as a negative regulator. Our Greiss assay data demonstrated that transfection of miR‐155 mimics into human hepatocytes significantly inhibited cytokine‐induced NO level. miRNA mimics with random similar sequence served as negative control had no effect. Furthermore, transfection of miR‐155 inhibitors did not further induce hiNOS gene to produce more amount of NO. Surprisingly, human iNOS gene is not predicted as the direct target gene of miR‐155. Therefore, miR‐155 might target at the hiNOS‐upstream regulator to indirectly suppress hiNOS gene expression.