Prokineticin 2 Plays a Pivotal Role in Psoriasis

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ID: 55881
2016
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Abstract
Psoriasis is histologically characterized by keratinocytes (KC) hyperproliferation, inflammation, and increased angiogenesis, but the pathological factor responsible for these symptoms is unknown. Here, a neuroendocrine peptide (prokineticin 2, PK2), is highly expressed in human and mouse psoriatic skins but no significant change in other autoimmune diseases, suggesting that PK2 is a psoriasis-specific factor. Bacterial products significantly up-regulated PK2, implying that infection induces PK2 over-expression. PK2 promoted KC and macrophage to produce interleukin-1 (IL-1), the central player of inflammation and psoriasis, which acts on adjacent fibroblast to induce inflammatory cascades and KC hyperproliferation. IL-1 feeds back on macrophages to induce PK2 production to perpetuate PK2-IL-1 positive feedback loop. PK2 also promoted angiogenesis, another psoriatic symptom. In mouse models, PK2 over-expression aggravated psoriasis while its knock-down inhibited pathological development. The results indicate that PK2 over-production perpetuates psoriatic symptoms by creating PK-2-IL-1 vicious loop. PK2 is a central player in psoriasis and a promising psoriasis-specific target.
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he2016prokineticinebiomedicine Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors He, Xiaoqin;Shen, Chuanbin;Lu, Qiumin;Li, Jiong;Wei, Yuquan;He, Li;Bai, Ruizhen;Zheng, Jie;Luan, Ning;Zhang, Zhiye;Rong, Mingqiang;Lai, Ren;
Journal ebiomedicine
Year 2016
DOI
DOI not found
URL
http://www.sciencedirect.com/science/article/pii/S2352396416304832
Keywords
Biology (General) Medicine Chemical technology

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