miR-383 reduces keratinocyte proliferation and induces the apoptosis in psoriasis via disruption of LCN2-dependent JAK/STAT pathway activation.

Psoriasis is a chronic and relapsing disorder with considerable negative effects on patients' quality of life. The finer details associated with the molecular mechanism of psoriasis and its pathogenesis remain somewhat elusive. Extensive studies have highlighted the crucial role of microRNAs (miRNAs) in the development of psoriasis. Hence, the current study aimed to investigate the effect of miR-383 on a psoriasis rat model and elucidate the underlying molecular mechanism. The rat psoriasis model was established via imiquimod (IMQ) induction followed by verification of miR-383 and LCN2 expression in the skin tissues of the models. ELISA was conducted to determine the secretion of inflammatory factors. Keratinocyte proliferation and apoptosis was evaluated by MTT assay and flow cytometric analysis. Down-regulation of miR-383 and up-regulation of LCN2 were detected in the psoriasis rat model. Our data indicated that miR-383 targeted LCN2 by binding to its 3'UTR and inhibited JAK/STAT pathway activation. Notably, miR-383 overexpression or LCN2 knockdown attenuated psoriasis-like symptoms, suppressed inflammatory response, reduced the expression of JAK3 and STAT3, ceased keratinocyte proliferation, and promoted the apoptosis. The findings of our study suggest that miR-383 may inhibit LCN2 and inactivate the JAK/STAT pathway, suppressing the progression of psoriasis in a rat model. This study provided novel insights into the pathogenesis of psoriasis and offered potential targets for psoriasis treatment.