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Activation of dopamine D1 receptor decreased NLRP3-mediated inflammation in intracerebral hemorrhage mice

Overview of attention for article published in Journal of Neuroinflammation, January 2018
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2 tweeters

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39 Mendeley
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Title
Activation of dopamine D1 receptor decreased NLRP3-mediated inflammation in intracerebral hemorrhage mice
Published in
Journal of Neuroinflammation, January 2018
DOI 10.1186/s12974-017-1039-7
Pubmed ID
Authors

Tian Wang, Derek Nowrangi, Lingyan Yu, Tai Lu, Jiping Tang, Bing Han, Yuxin Ding, Fenghua Fu, John H. Zhang

Abstract

Inflammasomes are involved in diverse inflammatory diseases. Previous study reported that the neurotransmitter dopamine inhibited NLRP3 inflammasome activation via dopamine D1 receptor (DRD1). The present study aims to investigate the role of DRD1 on neuroinflammation in intracerebral hemorrhage (ICH) mice and the potential mechanism mediated by NLRP3 inhibition. One hundred and six male CD-1 mice were subjected to intrastriatal injection of bacterial collagenase or PBS. A68930 (DRD1 specific agonist) was administered by subcutaneous injection at 1 h after collagenase injection. Behavioral deficits and brain water content were assayed. The expression of Iba 1 and MPO levels were measured by immunofluorescence staining. The expressions of proteins in the DRD1/interferon-beta (IFN-beta)/NLRP3 signaling pathway were evaluated by western blotting. Activation of the DRD1 by A68930 decreased brain edema and improved behavior at 24 and 72 h of ICH. A68930 inhibited partly the activation of microglia and the neutrophil infiltration after 24 h of ICH. IFN-beta, p-STAT1 increased while NLRP3, caspase 1, and IL-1beta decreased after A68930 administration in ICH mice. DRD1 antagonist and IFN-beta siRNA reversed effects of A68930 on neurological outcome and brain edema. DRD1 antagonist and IFN-beta siRNA blocked not only A68930-mediated increases of IFN-beta, p-STAT1 but also A68930-mediated decreases of NLRP3, caspase 1, and IL-1beta. DRD1 activation by A68930 improves neurological outcome through inhibition of NLRP3-mediated inflammation in ICH mice.

Twitter Demographics

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Mendeley readers

The data shown below were compiled from readership statistics for 39 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 39 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 12 31%
Researcher 5 13%
Student > Master 5 13%
Professor > Associate Professor 3 8%
Student > Bachelor 3 8%
Other 3 8%
Unknown 8 21%
Readers by discipline Count As %
Neuroscience 14 36%
Medicine and Dentistry 5 13%
Pharmacology, Toxicology and Pharmaceutical Science 4 10%
Immunology and Microbiology 3 8%
Agricultural and Biological Sciences 3 8%
Other 1 3%
Unknown 9 23%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 09 January 2018.
All research outputs
#9,487,655
of 12,341,908 outputs
Outputs from Journal of Neuroinflammation
#943
of 1,420 outputs
Outputs of similar age
#233,467
of 354,255 outputs
Outputs of similar age from Journal of Neuroinflammation
#69
of 136 outputs
Altmetric has tracked 12,341,908 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,420 research outputs from this source. They receive a mean Attention Score of 4.9. This one is in the 28th percentile – i.e., 28% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 354,255 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 28th percentile – i.e., 28% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 136 others from the same source and published within six weeks on either side of this one. This one is in the 38th percentile – i.e., 38% of its contemporaries scored the same or lower than it.