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The role of microglial P2X7: modulation of cell death and cytokine release

Overview of attention for article published in Journal of Neuroinflammation, July 2017
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • Good Attention Score compared to outputs of the same age (74th percentile)
  • Good Attention Score compared to outputs of the same age and source (76th percentile)

Mentioned by

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1 news outlet

Citations

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126 Dimensions

Readers on

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149 Mendeley
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Title
The role of microglial P2X7: modulation of cell death and cytokine release
Published in
Journal of Neuroinflammation, July 2017
DOI 10.1186/s12974-017-0904-8
Pubmed ID
Authors

Yingbo He, Natalie Taylor, Lawrence Fourgeaud, Anindya Bhattacharya

Abstract

ATP-gated P2X7 is a non-selective cation channel, which participates in a wide range of cellular functions as well as pathophysiological processes including neuropathic pain, immune response, and neuroinflammation. Despite its abundant expression in microglia, the role of P2X7 in neuroinflammation still remains unclear. Primary microglia were isolated from cortices of P0-2 C57BL/6 wild-type or P2X7 knockout (P2X7(-/-)) mouse pups. Lipopolysaccharide, lipopolysaccharide plus IFNγ, or IL4 plus IL13 were used to polarize microglia to pro-inflammatory or anti-inflammatory states. P2rx7 expression level in resting or activated mouse and human microglia was measured by RNA-sequencing and quantitative real-time PCR. Microglial cell death was measured by cell counting kit-8 and immunocytochemistry, and microglial secretion in wild-type or P2X7(-/-) microglia was examined by Luminex multiplex assay or ELISA using P2X7 agonist BzATP or P2X7 antagonist A-804598. P2X7 signaling was analyzed by Western blot. First, we confirmed that P2rx7 is constitutively expressed in mouse and human primary microglia. Moreover, P2rx7 mRNA level was downregulated in mouse microglia under both pro- and anti-inflammatory conditions. Second, P2X7 agonist BzATP caused cell death of mouse microglia, while this effect was suppressed either by P2X7 knockout or by A-804598 under both basal and pro-inflammatory conditions, which suggests the mediating role of P2X7 in BzATP-induced microglial cell death. Third, BzATP-induced release of IL1 family cytokines including IL1α, IL1β, and IL18 was blocked in P2X7(-/-) microglia or by A-804598 in pro-inflammatory microglia, while the release of other cytokines/chemokines was independent of P2X7 activation. These findings support the specific role of P2X7 in IL1 family cytokine release. Finally, P2X7 activation was discovered to be linked to AKT and ERK pathways, which may be the underlying mechanism of P2X7 functions in microglia. These results reveal that P2X7 mediates BzATP-induced microglial cell death and specific release of IL1 family cytokines, indicating the important role of P2X7 in neuroinflammation and implying the potential of targeting P2X7 for the treatment of neuroinflammatory disorders.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 149 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 149 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 38 26%
Student > Bachelor 18 12%
Researcher 16 11%
Student > Master 13 9%
Student > Doctoral Student 7 5%
Other 10 7%
Unknown 47 32%
Readers by discipline Count As %
Neuroscience 30 20%
Biochemistry, Genetics and Molecular Biology 17 11%
Immunology and Microbiology 11 7%
Agricultural and Biological Sciences 11 7%
Medicine and Dentistry 11 7%
Other 17 11%
Unknown 52 35%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 7. 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 12 May 2023.
All research outputs
#4,399,294
of 23,751,351 outputs
Outputs from Journal of Neuroinflammation
#841
of 2,738 outputs
Outputs of similar age
#68,588
of 284,360 outputs
Outputs of similar age from Journal of Neuroinflammation
#10
of 51 outputs
Altmetric has tracked 23,751,351 research outputs across all sources so far. Compared to these this one has done well and is in the 80th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 2,738 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.8. This one has gotten more attention than average, scoring higher than 64% of its peers.
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 284,360 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 74% of its contemporaries.
We're also able to compare this research output to 51 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 76% of its contemporaries.