LAUSR

Psoriasis is a common inflammatory skin disease, but the exact pathogenesis is largely unknown. Interleukin‐22 (IL‐22) has demonstrated its vital role in T‐cell‐mediated immune response by interacting with keratinocytes in the pathogenesis of psoriasis. Here, we showed the differentially expressed miRNAs and their potential targets in HaCaT cells stimulated by IL‐22 using miRNA and mRNA microarrays. We revealed a total of 20 significantly changed (more than twofold) miRNAs in HaCaT cells and validated the results with quantitative reverse transcriptase PCR (qRT‐PCR). We demonstrated that miR‐122‐5p was up‐regulated both in HaCaT cells stimulated by IL‐22 and in psoriatic lesions. Then, we aimed to investigate the biological roles and potential mechanism of miR‐122‐5p in keratinocytes. As a result, CCK‐8 assay indicated that overexpression of miR‐122‐5p in keratinocytes promoted proliferation and conversely inhibition of endogenous miR‐122‐5p suppressed proliferation. According to the microarray analysis, we assumed that Sprouty2 (Spry2), a negative regulator of extracellular signal regulated kinase/mitogen‐activated protein kinase signalling pathway, was a direct target gene of miR‐122‐5p. We found that the staining of Spry2 in cytoplasm was mainly localized in both basal and suprabasal layers of epidermis and showed a markedly decreased expression in psoriasis than in normal control by immunohistochemistry. Luciferase reporter and Western blot assays in HaCaT cells demonstrated that Spry2 was a direct target gene of miR‐122‐5p. In conclusion, IL‐22‐induced miR‐122‐5p promotes keratinocyte proliferation possibly by downregulating the expression of Spry2 thus playing important roles in the pathogenesis of psoriasis.