Sep 24, 2017
Caixia Li; Xiaocui Bai; Yuchen Zhuang; Shuai Shao; Gang Wang
Latest epidemiological investigations suggest patients with psoriasis have an increased risk of developing metabolic consequences. C1q/TNF-related proteins-3 (CTRP3) is an important newly identified adipokine as a cardio-protective factor and regulator of glucose homeostasis which is mainly produced by mature adipocytes. Here we demonstrated that CTRP3 could regulate imiquimod-induced psoriasis-like skin inflammation. Balb/c mice treated with recombinant mouse CTRP3 showed alleviative disease phenotype and decreased epidermis thickness compared with non-CTRP3 treated psoriatic mice. QRT-PCR assay indicated that the production of IL-17A, IL-8, and CXCL1 were decreased expressed by keratinocyte isolated from CTRP3 treated mice. Then we cultured human keratinocyte HaCaT cells and added IFN-γ, TNF-α, IL-17A and IL-22 to simulate the inflammatory environment of psoriasis epidermis in vitro. We found CTRP3 can inhibit the over-proliferation of HaCaT cells induced by the compound cytokines mentioned before. The inflammatory cytokines and chemokines were also down regulated in the CTRP3-protective group compared with compound cytokines cells. Then we found serum levels of CTRP3 in patients of psoriasis were significantly lower compared with age and sex matched healthy controls. Additionally, CTRP3 levels were reduced in moderate-to-server psoriasis patients and alcoholic individuals. We further detected the CTRP3 levels were rescued after systemic treatment in the in-patient department. Furthermore, we discovered the expression of CTRP3 during pre-adipocyte differentiation and maturation could be down regulated by TNF-α not IL-17A nor IL-22. In summary, our findings demonstrated the possible therapeutically effect of CTRP3 in the pathogenesis of psoriasis which would imply a mechanism underlying relationship between psoriasis and metabolic and cardiovascular disorders.
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