Abstract
AbstractBackgroundPsoriasis is a common chronic inflammatory skin disease characterized by epidermal hyperplasia, inflammatory cell infiltration and excessive neovascularization. It was previously found that C10orf99 regulates keratinocyte proliferation and inflammation in psoriasis. However, the role of C10orf99 on angiogenesis associated with psoriasis is unknown.MethodsWe used imiquimod (IMQ)‐induced psoriasis mice and M5‐induced cellular model of psoriasis to research the effects of C10orf99 knockdown on angiogenesis in psoriasis in vivo and in vitro.ResultsIn this study, our data showed that C10orf99 knockdown ameliorated imiquimod (IMQ)‐induced red plaques in mice and reduced the number of microvessels. Furthermore, we found such an effect was achieved by down‐regulating the expression of vascular endothelial growth factor (VEGF) and metallomatrix proteinase 2 (MMP2). Consistently, C10orf99 knockdown significantly downgraded the expression of MMP2 and VEGF in cellular model of psoriasis.ConclusionThese results suggested that C10orf99 could regulate angiogenesis in psoriasis and it might be a promising potential target of psoriasis.
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