Inhibition of miR-155 Attenuates CD14(+) Monocyte-Mediated Inflammatory Response and Oxidative Stress in Psoriasis Through TLR4/MyD88/NF-κB Signaling Pathway

PURPOSE: Previous studies showed the link of CD14(+) monocytes to inflammation and oxidation in psoriasis. In the present study, we investigated the regulatory role of miR-155 in CD14(+) monocyte function in psoriasis. MATERIALS AND METHODS: CD14(+) monocytes were isolated from peripheral blood by magnetic bead separation method and its function was assessed following silence of miR-155 by lentivirus transfection with or without inhibition of TLR4 pathway. CCK8 and EdU were used to assess the proliferation of CD14(+) monocytes. Expression levels of SOCS1, TLR4 and MyD88 proteins were determined by Western blotting, while expression levels of IL-6, TNF-α, ROS, MDA and T-AOC were measured by ELISA kit. The expression levels of mRNA for miR-155, NF-κB and its subunit NF-κB-p65 were assessed by q-PCR. RESULTS: The results showed that compared with normal control CD14(+) monocytes, the expression levels of miR-155, NF-κB and NF-κB-p65, TLR4, MyD88 and IL-6, TNF-α were increased, while expression levels of SOCS1 were decreased in CD14(+) monocytes from psoriatic patients. Enhanced cell proliferation and oxidation were also observed in CD14(+) monocytes from psoriatic patients. Inhibition of miR-155 partially corrected the abnormalities of cell proliferation and expression levels of biomarkers mentioned above in CD14(+) monocytes from psoriatic patients. Inhibitions of both TLR4 pathway and miR-155 further corrected abnormalities of proliferation and the above biomarkers in CD14(+) monocytes from psoriatic patients. CONCLUSION: These results suggest that increased expression levels of miR-155 contribute to CD14(+) monocyte-mediated inflammation and oxidation in psoriasis via TLR4 pathway.