miR-146b correlates with increased disease activity and psoriatic tissue inflammation and promotes keratinocyte proliferation in psoriasis.

The present study aimed to investigate the expression of microRNA (miR)-146b in psoriatic tissue and its correlation with psoriasis activity and inflammation. The effect of miR-146b overexpression on keratinocyte proliferation and apoptosis was also explored. The expression of miR-146b in the psoriasis-affected tissue and non-affected tissue of 110 patients was determined via reverse transcription-quantitative (RT-q)PCR. The psoriasis-affected body surface area and psoriasis area severity index (PASI) score were recorded for evaluating disease activity. The expression of various inflammatory cytokines in psoriasis-affected tissue was also detected via RT-qPCR. miR-146b overexpression and control plasmids were constructed and transfected into HaCaT cells . Subsequently, cell proliferation, apoptosis and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-induced cell apoptosis were determined. The results revealed that the expression of miR-146b was increased in psoriasis-affected tissue compared with that in unaffected tissue. The results obtained from a receiver operating characteristic curve analysis demonstrated that miR-146b levels were able to discriminate between psoriasis-affected tissue and unaffected tissue, with an area under the curve value of 0.781 (95% CI: 0.720-0.843). In addition, miR-146b expression in psoriatic tissue was correlated with an increased PASI score in patients with psoriasis. miR-146b expression in psoriatic tissue was positively correlated with TNF-α, interleukin (IL)-6 and IL-17 mRNA levels. , miR-146b overexpression enhanced HaCaT cell proliferation and suppressed apoptosis as well as TRAIL-induced apoptosis when compared with that in control-transfected HaCaT cells. In conclusion, miR-146b was positively correlated with disease activity and psoriatic tissue inflammation. Keratinocyte proliferation was also promoted in psoriasis.