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The lncRNA Neat1 promotes activation of inflammasomes in macrophages

Author

Listed:
  • Pengfei Zhang

    (University of Science and Technology of China)

  • Limian Cao

    (University of Science and Technology of China)

  • Rongbin Zhou

    (University of Science and Technology of China)

  • Xiaolu Yang

    (University of Pennsylvania)

  • Mian Wu

    (University of Science and Technology of China
    School of Clinical Medicine, Henan University)

Abstract

The inflammasome has an essential function in innate immune, responding to a wide variety of stimuli. Here we show that the lncRNA Neat1 promotes the activation of several inflammasomes. Neat1 associates with the NLRP3, NLRC4, and AIM2 inflammasomes in mouse macrophages to enhance their assembly and subsequent pro-caspase-1 processing. Neat1 also stabilizes the mature caspase-1 to promote interleukin-1β production and pyroptosis. Upon stimulation with inflammasome-activating signals, Neat1, which normally resides in the paraspeckles, disassociates from these nuclear bodies and translocates to the cytoplasm to modulate inflammasome activation using above mechanism. Neat1 is also up-regulated under hypoxic conditions in a HIF-2α-dependent manner, mediating the effect of hypoxia on inflammasomes. Moreover, in the mouse models of peritonitis and pneumonia, Neat1 deficiency significantly reduces inflammatory responses. These results reveal a previously unrecognized role of lncRNAs in innate immunity, and suggest that Neat1 is a common mediator for inflammasome stimuli.

Suggested Citation

  • Pengfei Zhang & Limian Cao & Rongbin Zhou & Xiaolu Yang & Mian Wu, 2019. "The lncRNA Neat1 promotes activation of inflammasomes in macrophages," Nature Communications, Nature, vol. 10(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-09482-6
    DOI: 10.1038/s41467-019-09482-6
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