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Dopamine Controls Systemic Inflammation through Inhibition of NLRP3 Inflammasome

Cell, 2015-01, Vol.160 (1-2), p.62-73 [Peer Reviewed Journal]

2015 Elsevier Inc. ;Copyright © 2015 Elsevier Inc. All rights reserved. ;ISSN: 0092-8674 ;EISSN: 1097-4172 ;DOI: 10.1016/j.cell.2014.11.047 ;PMID: 25594175

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  • Title:
    Dopamine Controls Systemic Inflammation through Inhibition of NLRP3 Inflammasome
  • Author: Yan, Yiqing ; Jiang, Wei ; Liu, Lei ; Wang, Xiaqiong ; Ding, Chen ; Tian, Zhigang ; Zhou, Rongbin
  • Subjects: Animals ; Autophagy ; Carrier Proteins - metabolism ; Cyclic AMP - metabolism ; Dopamine - metabolism ; Inflammasomes - immunology ; Inflammation - immunology ; Mice ; Mice, Inbred C57BL ; Neurotransmitter Agents - metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein ; Protein Aggregates ; Receptors, Dopamine - genetics ; Receptors, Dopamine - metabolism ; Receptors, Dopamine D1 ; Signal Transduction ; Ubiquitination
  • Is Part Of: Cell, 2015-01, Vol.160 (1-2), p.62-73
  • Description: Inflammasomes are involved in diverse inflammatory diseases, so the activation of inflammasomes needs to be tightly controlled to prevent excessive inflammation. However, the endogenous regulatory mechanisms of inflammasome activation are still unclear. Here, we report that the neurotransmitter dopamine (DA) inhibits NLRP3 inflammasome activation via dopamine D1 receptor (DRD1). DRD1 signaling negatively regulates NLRP3 inflammasome via a second messenger cyclic adenosine monophosphate (cAMP), which binds to NLRP3 and promotes its ubiquitination and degradation via the E3 ubiquitin ligase MARCH7. Importantly, in vivo data show that DA and DRD1 signaling prevent NLRP3 inflammasome-dependent inflammation, including neurotoxin-induced neuroinflammation, LPS-induced systemic inflammation, and monosodium urate crystal (MSU)-induced peritoneal inflammation. Taken together, our results reveal an endogenous mechanism of inflammasome regulation and suggest DRD1 as a potential target for the treatment of NLRP3 inflammasome-driven diseases. [Display omitted] •Dopamine and DRD1 signaling inhibits NLRP3 inflammasome activation•Dopamine and DRD1 signaling induce NLRP3 ubiquitination and degradation via cAMP•cAMP promotes NLRP3 ubiquitination via E3 ligase MARCH7•Dopamine and DRD1 signaling control systemic inflammation via inhibiting inflammasome The dysregulation of NLRP3 inflammasome contributes to many inflammation-associated diseases. Yan et al. now find that dopamine and DRD1 signaling function as an endogenous restrictor of NLRP3 inflammasome activation and can control both neuroinflammation and periphery inflammation via promoting NLRP3 ubiquitination and degradation, suggesting that DRD1 might be a new target for treatment of NLRP3 inflammasome-driven inflammatory diseases.
  • Publisher: United States: Elsevier Inc
  • Language: English
  • Identifier: ISSN: 0092-8674
    EISSN: 1097-4172
    DOI: 10.1016/j.cell.2014.11.047
    PMID: 25594175
  • Source: Cell Press Free Archives
    MEDLINE
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