NF-κB-induced microRNA-31 promotes epidermal hyperplasia by repressing protein phosphatase 6 in psoriasis

  • Sha Yan
  • , Zhenyao Xu
  • , Fangzhou Lou
  • , Lingyun Zhang
  • , Fang Ke
  • , Jing Bai
  • , Zhaoyuan Liu
  • , Jinlin Liu
  • , Hong Wang*
  • , Huiyuan Zhu
  • , Yang Sun
  • , Wei Cai
  • , Yuanyuan Gao
  • , Bing Su
  • , Qun Li
  • , Xiao Yang
  • , Jianxiu Yu
  • , Yuping Lai
  • , Xue Zhong Yu
  • , Yan Zheng
  • Nan Shen, Y. Eugene Chin, Honglin Wang
*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

214 Scopus citations

Abstract

NF-κB is constitutively activated in psoriatic epidermis. However, how activated NF-κB promotes keratinocyte hyperproliferation in psoriasis is largely unknown. Here we report that the NF-κB activation triggered by inflammatory cytokines induces the transcription of microRNA (miRNA) miR-31, one of the most dynamic miRNAs identified in the skin of psoriatic patients and mouse models. The genetic deficiency of miR-31 in keratinocytes inhibits their hyperproliferation, decreases acanthosis and reduces the disease severity in psoriasis mouse models. Furthermore, protein phosphatase 6 (ppp6c), a negative regulator that restricts the G1 to S phase progression, is diminished in human psoriatic epidermis and is directly targeted by miR-31. The inhibition of ppp6c is functionally important for miR-31-mediated biological effects. Moreover, NF-κB activation inhibits ppp6c expression directly through the induction of miR-31, and enhances keratinocyte proliferation. Thus, our data identify NF-κB-induced miR-31 and its target, ppp6c, as critical factors for the hyperproliferation of epidermis in psoriasis.

Original languageEnglish
Article number7652
JournalNature Communications
Volume6
DOIs
StatePublished - 3 Jul 2015

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