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Peli1 Contributions in Microglial Activation, Neuroinflammatory Responses and Neurological Deficits Following Experimental Subarachnoid Hemorrhage

Overview of attention for article published in Frontiers in Molecular Neuroscience, November 2017
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Title
Peli1 Contributions in Microglial Activation, Neuroinflammatory Responses and Neurological Deficits Following Experimental Subarachnoid Hemorrhage
Published in
Frontiers in Molecular Neuroscience, November 2017
DOI 10.3389/fnmol.2017.00398
Pubmed ID
Authors

Xue-Ping Huang, Jian-Hua Peng, Jin-Wei Pang, Xiao-Cui Tian, Xin-Shen Li, Yue Wu, Yong Li, Yong Jiang, Xiao-Chuan Sun

Abstract

Early brain injury (EBI) following subarachnoid hemorrhage (SAH) is closely associated with neuroinflammation. Microglial activation is an early event that leads to neuroinflammation after SAH. Peli1 is an E3 ubiquitin ligase that mediates the induction of pro-inflammatory cytokines in microglia. Here we report Peli1 contributions in SAH mediated brain pathology. An SAH model was induced by endovascular perforation in adult male C57BL/6J mice. Peli1 was markedly induced in mice brains in a time-dependent manner and was predominantly expressed in CD16/32-positive microglia after SAH. Using genetic approaches, we demonstrated that decreased Peli1 significantly improved neurological deficits, attenuated brain edema, reduced over-expression of pro-inflammatory cytokine IL-6 and modified apoptotic/antiapoptotic biomarkers. In addition, Peli1 downregulation suppressed ERK and JNK phosphorylation levels via the downregulation of cIAP1/2 expression, subsequently reducing inducible nitric oxide synthase (iNOS) expression after SAH. Therefore, these findings demonstrate that Peli1 contributes to microglia-mediated neuroinflammation in EBI by mediating cIAP1/2 activation, thus promoting the activation of MyD88-dependent MAPK pathway after experimental SAH. Our findings also showed that Peli1 could promote the expression of M1 microglia polarization biomarker CD16/32 and iNOS after SAH. Targeting Peli1 exerts neuroprotective effects during EBI after SAH, thus could provide potential option for prevention-therapy in high-risk individuals.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 16 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 16 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 25%
Student > Doctoral Student 2 13%
Lecturer > Senior Lecturer 1 6%
Student > Bachelor 1 6%
Researcher 1 6%
Other 0 0%
Unknown 7 44%
Readers by discipline Count As %
Neuroscience 5 31%
Medicine and Dentistry 3 19%
Unknown 8 50%
Attention Score in Context

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 12 December 2017.
All research outputs
#20,454,971
of 23,011,300 outputs
Outputs from Frontiers in Molecular Neuroscience
#2,492
of 2,910 outputs
Outputs of similar age
#372,982
of 437,917 outputs
Outputs of similar age from Frontiers in Molecular Neuroscience
#102
of 123 outputs
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So far Altmetric has tracked 2,910 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.7. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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