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Oxidative stress-induced FABP5 S-glutathionylation protects against acute lung injury by suppressing inflammation in macrophages

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  • Yuxian Guo

    (Zhejiang University School of Medicine
    Zhejiang University School of Medicine)

  • Yaru Liu

    (Zhejiang University School of Medicine)

  • Shihao Zhao

    (Zhejiang University School of Medicine)

  • Wangting Xu

    (Zhejiang University School of Medicine)

  • Yiqing Li

    (Zhejiang University School of Medicine)

  • Pengwei Zhao

    (Zhejiang University School of Medicine)

  • Di Wang

    (Zhejiang University School of Medicine)

  • Hongqiang Cheng

    (Zhejiang University School of Medicine
    Zhejiang University School of Medicine)

  • Yuehai Ke

    (Zhejiang University School of Medicine
    Zhejiang University School of Medicine
    Zhejiang University Medical Center)

  • Xue Zhang

    (Zhejiang University School of Medicine
    Zhejiang University School of Medicine)

Abstract

Oxidative stress contributes to the pathogenesis of acute lung injury. Protein S-glutathionylation plays an important role in cellular antioxidant defense. Here we report that the expression of deglutathionylation enzyme Grx1 is decreased in the lungs of acute lung injury mice. The acute lung injury induced by hyperoxia or LPS is significantly relieved in Grx1 KO and Grx1fl/flLysMcre mice, confirming the protective role of Grx1-regulated S-glutathionylation in macrophages. Using a quantitative redox proteomics approach, we show that FABP5 is susceptible to S-glutathionylation under oxidative conditions. S-glutathionylation of Cys127 in FABP5 promotes its fatty acid binding ability and nuclear translocation. Further results indicate S-glutathionylation promotes the interaction of FABP5 and PPARβ/δ, activates PPARβ/δ target genes and suppresses the LPS-induced inflammation in macrophages. Our study reveals a molecular mechanism through which FABP5 S-glutathionylation regulates macrophage inflammation in the pathogenesis of acute lung injury.

Suggested Citation

  • Yuxian Guo & Yaru Liu & Shihao Zhao & Wangting Xu & Yiqing Li & Pengwei Zhao & Di Wang & Hongqiang Cheng & Yuehai Ke & Xue Zhang, 2021. "Oxidative stress-induced FABP5 S-glutathionylation protects against acute lung injury by suppressing inflammation in macrophages," Nature Communications, Nature, vol. 12(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-27428-9
    DOI: 10.1038/s41467-021-27428-9
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    1. Youdong Pan & Tian Tian & Chang Ook Park & Serena Y. Lofftus & Shenglin Mei & Xing Liu & Chi Luo & John T. O’Malley & Ahmed Gehad & Jessica E. Teague & Sherrie J. Divito & Robert Fuhlbrigge & Pere Pui, 2017. "Survival of tissue-resident memory T cells requires exogenous lipid uptake and metabolism," Nature, Nature, vol. 543(7644), pages 252-256, March.
    2. Liraz Levi & Zeneng Wang & Mary Kathryn Doud & Stanley L. Hazen & Noa Noy, 2015. "Saturated fatty acids regulate retinoic acid signalling and suppress tumorigenesis by targeting fatty acid-binding protein 5," Nature Communications, Nature, vol. 6(1), pages 1-10, December.
    3. Chun-An Chen & Tse-Yao Wang & Saradhadevi Varadharaj & Levy A. Reyes & Craig Hemann & M. A. Hassan Talukder & Yeong-Renn Chen & Lawrence J. Druhan & Jay L. Zweier, 2010. "S-glutathionylation uncouples eNOS and regulates its cellular and vascular function," Nature, Nature, vol. 468(7327), pages 1115-1118, December.
    4. William J. Mach & Amanda R. Thimmesch & J. Thomas Pierce & Janet D. Pierce, 2011. "Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung," Nursing Research and Practice, Hindawi, vol. 2011, pages 1-7, June.
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