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Neuraminidase 1 promotes renal fibrosis development in male mice

Author

Listed:
  • Qian-Qian Chen

    (China Pharmaceutical University
    Nanjing University of Chinese Medicine)

  • Kang Liu

    (The First Affiliated Hospital of Nanjing Medical University)

  • Ning Shi

    (China Pharmaceutical University)

  • Gaoxiang Ma

    (China Pharmaceutical University)

  • Peipei Wang

    (Shanghai Ocean University)

  • Hua-Mei Xie

    (China Pharmaceutical University)

  • Si-Jia Jin

    (China Pharmaceutical University)

  • Ting-Ting Wei

    (China Pharmaceutical University)

  • Xiang-Yu Yu

    (China Pharmaceutical University)

  • Yi Wang

    (China Pharmaceutical University)

  • Jun-Yuan Zhang

    (China Pharmaceutical University)

  • Ping Li

    (China Pharmaceutical University)

  • Lian-Wen Qi

    (China Pharmaceutical University
    China Pharmaceutical University
    China Pharmaceutical University)

  • Lei Zhang

    (China Pharmaceutical University
    China Pharmaceutical University)

Abstract

The functions of the influenza virus neuraminidase has been well documented but those of the mammalian neuraminidases remain less explored. Here, we characterize the role of neuraminidase 1 (NEU1) in unilateral ureteral obstruction (UUO) and folic acid (FA)-induced renal fibrosis mouse models. We find that NEU1 is significantly upregulated in the fibrotic kidneys of patients and mice. Functionally, tubular epithelial cell-specific NEU1 knockout inhibits epithelial-to-mesenchymal transition, inflammatory cytokines production, and collagen deposition in mice. Conversely, NEU1 overexpression exacerbates progressive renal fibrosis. Mechanistically, NEU1 interacts with TGFβ type I receptor ALK5 at the 160-200aa region and stabilizes ALK5 leading to SMAD2/3 activation. Salvianolic acid B, a component of Salvia miltiorrhiza, is found to strongly bind to NEU1 and effectively protect mice from renal fibrosis in a NEU1-dependent manner. Collectively, this study characterizes a promotor role for NEU1 in renal fibrosis and suggests a potential avenue of targeting NEU1 to treat kidney diseases.

Suggested Citation

  • Qian-Qian Chen & Kang Liu & Ning Shi & Gaoxiang Ma & Peipei Wang & Hua-Mei Xie & Si-Jia Jin & Ting-Ting Wei & Xiang-Yu Yu & Yi Wang & Jun-Yuan Zhang & Ping Li & Lian-Wen Qi & Lei Zhang, 2023. "Neuraminidase 1 promotes renal fibrosis development in male mice," Nature Communications, Nature, vol. 14(1), pages 1-20, December.
    • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-37450-8
    DOI: 10.1038/s41467-023-37450-8
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    References listed on IDEAS

    as
    1. Ida Annunziata & Annette Patterson & Danielle Helton & Huimin Hu & Simon Moshiach & Elida Gomero & Ralph Nixon & Alessandra d’Azzo, 2013. "Lysosomal NEU1 deficiency affects amyloid precursor protein levels and amyloid-β secretion via deregulated lysosomal exocytosis," Nature Communications, Nature, vol. 4(1), pages 1-12, December.
    2. Sebastian Schafer & Sivakumar Viswanathan & Anissa A. Widjaja & Wei-Wen Lim & Aida Moreno-Moral & Daniel M. DeLaughter & Benjamin Ng & Giannino Patone & Kingsley Chow & Ester Khin & Jessie Tan & Sonia, 2017. "IL-11 is a crucial determinant of cardiovascular fibrosis," Nature, Nature, vol. 552(7683), pages 110-115, December.
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