Abstract: Objective: To investigate the expression of LCN2 in the cell/animal model of psoriasis and the effect of C10orf99 knockdown on the expression level of LCN2 in cultured HaCaT in vitro. Methods: Use imiquimod to eatablish the animal model of psoriais to verify the expression level of LCN2 in that model. Use M5 (IL-1α, IL-17, IL-22, TNFα and OSM) to stimulate HaCaT to establish the cell model of psoriasis and then use qRT-PCR and Western Blot to detect the expression of LCN2 in the model. C10orf99 shRNA lentivirus was used to knockdown the expression of C10orf99 and qRT-PCR and Western Blot were carried out to detect the effect of C10orf99 knockdown on the expression of LCN2 in cultured psoriatic HaCaT in vitro. Results: The expression of LCN2 in the models of psoriasis is significantly increased. In additon, to be compared with the control group, the knockdown of C10orf99 significantly decreases the expression of LCN2 in the cell model of psoriasis (P<0.05). Conclusion: C10orf99 is involved in the pathogenesis of psoriasis via regulating the expression of LCN2.

Key words: psoriasis, HaCaT, C10orf99, LCN2