Prokineticin 2 Plays a Pivotal Role in Psoriasis

Xiaoqin He, Chuanbin Shen, Qiumin Lu, Jiong Li, Yuquan Wei, Li He, Ruizhen Bai, Jie Zheng, Ning Luan, Zhiye Zhang, Mingqiang Rong, Ren Lai

Research output: Contribution to journalArticle

10 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)248-261
Number of pages14
JournalEBioMedicine
Volume13
DOIs
StatePublished - Nov 1 2016

Keywords

  • Angiogenesis
  • Cell proliferation
  • Inflammation
  • Interleukin-1
  • Prokineticin2
  • Psoriasis

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)

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  • Cite this

    He, X., Shen, C., Lu, Q., Li, J., Wei, Y., He, L., Bai, R., Zheng, J., Luan, N., Zhang, Z., Rong, M., & Lai, R. (2016). Prokineticin 2 Plays a Pivotal Role in Psoriasis. EBioMedicine, 13, 248-261. https://doi.org/10.1016/j.ebiom.2016.10.022