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    Fc-Elabela fusion protein attenuates lipopolysaccharide-induced kidney injury in mice

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    Author
    Xu, Feng
    Zhou, Huifen
    Wu, Man
    Zhang, Hong
    Zhang, Yixian
    Zhao, Qingbin
    Brown, Robert
    Gong, Da-Wei
    Miao, Lining
    Date
    2020-09-30
    Journal
    Bioscience Reports
    Publisher
    Springer Nature
    Type
    Article
    
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    Show full item record
    See at
    https://doi.org/10.1042/BSR20192397
    Abstract
    Endotoxemia-induced acute kidney injury (AKI) is a common clinical condition that lacks effective treatments. Elabela (ELA) is a recently discovered kidney peptide hormone, encoded by the gene apela, and has been reported to improve cardio-renal outcomes in sepsis. However, ELA is a small peptide and is largely unsuitable for clinical use because of its short in vivo half-life. In the present study, we evaluated the potential renoprotective effects of a long-acting constant fragment (Fc)-ELA fusion protein in liposaccharide (LPS)-induced AKI in mice. LPS administration in mice for 5 days greatly lowered the gene expression of apela and impaired kidney function, as evidenced by elevated serum creatinine and the ratio of urine protein to creatinine. In addition, renal inflammation and macrophage infiltration were apparent in LPS-challenged mice. Treatment with the Fc-ELA fusion protein partially restored apela expression and attenuated the kidney inflammation. Moreover, LPS treatment induced reactive oxygen species (ROS) production and apoptosis in kidney HK-2 cells as well as in the mouse kidney, which were mitigated by ELA or Fc-ELA treatment. Finally, we found that ELA promoted the survival of HK-2 cells treated with LPS, and this action was abolished by LY204002, a PI3K/Akt inhibitor. Collectively, we have demonstrated that the Fc-ELA fusion protein has significant renoprotective activities against LPS-induced AKI in mice.
    Rights/Terms
    © 2020 The Author(s).
    Keyword
    Elabela (ELA)
    acute kidney injury (AKI)
    fusion protein
    liposaccharide (LPS)
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/13674
    ae974a485f413a2113503eed53cd6c53
    10.1042/BSR20192397
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