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

Author

Listed:
  • Sha Yan

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Zhenyao Xu

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Fangzhou Lou

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Lingyun Zhang

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Fang Ke

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Jing Bai

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Zhaoyuan Liu

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Jinlin Liu

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Hong Wang

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Huiyuan Zhu

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Yang Sun

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Wei Cai

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Yuanyuan Gao

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Bing Su

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Qun Li

    (Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Xiao Yang

    (State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology)

  • Jianxiu Yu

    (Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Yuping Lai

    (Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University)

  • Xue-Zhong Yu

    (Medical University of South Carolina)

  • Yan Zheng

    (The Second Affiliated Hospital of Xi’an Jiaotong University)

  • Nan Shen

    (Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Y. Eugene Chin

    (Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University School of Medicine (SJTU-SM))

  • Honglin Wang

    (Shanghai Institute of Immunology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM)
    Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine (SJTU-SM))

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.

Suggested Citation

  • 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 & Jian, 2015. "NF-κB-induced microRNA-31 promotes epidermal hyperplasia by repressing protein phosphatase 6 in psoriasis," Nature Communications, Nature, vol. 6(1), pages 1-15, November.
  • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8652
    DOI: 10.1038/ncomms8652
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    Cited by:

    1. Zhikai Wang & Yang Sun & Fangzhou Lou & Jing Bai & Hong Zhou & Xiaojie Cai & Libo Sun & Qianqian Yin & Sibei Tang & Yue Wu & Li Fan & Zhenyao Xu & Hong Wang & Xiaoyu Hu & Honglin Wang, 2022. "Targeting the transcription factor HES1 by L-menthol restores protein phosphatase 6 in keratinocytes in models of psoriasis," Nature Communications, Nature, vol. 13(1), pages 1-15, December.
    2. Xiangyu Lu & Le Kuai & Fang Huang & Jingsi Jiang & Jiankun Song & Yiqiong Liu & Si Chen & Lijie Mao & Wei Peng & Ying Luo & Yongyong Li & Haiqing Dong & Bin Li & Jianlin Shi, 2023. "Single-atom catalysts-based catalytic ROS clearance for efficient psoriasis treatment and relapse prevention via restoring ESR1," Nature Communications, Nature, vol. 14(1), pages 1-15, December.

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