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NLRP1 inflammasome is activated in patients with medial temporal lobe epilepsy and contributes to neuronal pyroptosis in amygdala kindling-induced rat model

Overview of attention for article published in Journal of Neuroinflammation, January 2015
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Title
NLRP1 inflammasome is activated in patients with medial temporal lobe epilepsy and contributes to neuronal pyroptosis in amygdala kindling-induced rat model
Published in
Journal of Neuroinflammation, January 2015
DOI 10.1186/s12974-014-0233-0
Pubmed ID
Authors

Chen-Chen Tan, Jian-Guo Zhang, Meng-Shan Tan, Hua Chen, Da-Wei Meng, Teng Jiang, Xiang-Fei Meng, Ying Li, Zhen Sun, Meng-Meng Li, Jin-Tai Yu, Lan Tan

Abstract

BackgroundTemporal lobe epilepsy (TLE) is often characterized pathologically by severe neuronal loss in the hippocampus. Understanding the mechanisms of neuron death is key to preventing the neurodegeneration associated with TLE. However, the involvement of neuronal loss to the epileptogenic process has yet to be fully determined. Recent studies have shown that the activation of NLRP1 can generate a functional caspase-1-containing inflammasome in vivo to drive the proinflammatory programmed cell death termed `pyroptosis¿, which has a key role in the pathogenesis of neurological disorders. To the best of our knowledge, there are no reported studies that performed detailed identification and validation of NLRP1 inflammasome during the epileptogenic process.MethodsWe first compared expression of NLRP1 and caspase-1 in resected hippocampus from patients with intractable mesial temporal lobe epilepsy (mTLE) with that of matched control samples. To further examine whether the activation of NLRP1 inflammasome contributes to neuronal pyroptosis, we employed a nonviral strategy to knock down the expression of NLRP1 and caspase-1 in the amygdala kindling-induced rat model. Proinflammatory cytokines levels and hippocampal neuronal loss were evaluated after 6 weeks of treatment in these NLRP1 or caspase-1 deficiency TLE rats.ResultsWestern blotting detected upregulated NLRP1 levels and active caspase-1 in mTLE patients in comparison to those levels seen in the controls, suggesting a role for this inflammasome in mTLE. Moreover, we employed direct in vivo infusion of nonviral small interfering RNA to knockdown NLRP1 or caspase-1 in the amygdala kindling-induced rat model, and discovered that these NLRP1 or caspase-1 silencing rats resulted in significantly reduced neuronal pyroptosis.ConclusionsOur data suggest that NLRP1/caspase-1 signaling participates in the seizure-induced degenerative process in humans and in the animal model of TLE and points to the silencing of NLRP1 inflammasome as a promising strategy for TLE therapy.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 104 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Spain 1 <1%
Unknown 103 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 21 20%
Student > Bachelor 16 15%
Student > Master 14 13%
Researcher 12 12%
Student > Doctoral Student 8 8%
Other 15 14%
Unknown 18 17%
Readers by discipline Count As %
Neuroscience 23 22%
Medicine and Dentistry 16 15%
Agricultural and Biological Sciences 15 14%
Biochemistry, Genetics and Molecular Biology 12 12%
Pharmacology, Toxicology and Pharmaceutical Science 7 7%
Other 8 8%
Unknown 23 22%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 01 February 2015.
All research outputs
#14,797,632
of 22,783,848 outputs
Outputs from Journal of Neuroinflammation
#1,649
of 2,624 outputs
Outputs of similar age
#197,848
of 352,967 outputs
Outputs of similar age from Journal of Neuroinflammation
#28
of 58 outputs
Altmetric has tracked 22,783,848 research outputs across all sources so far. This one is in the 32nd percentile – i.e., 32% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,624 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.6. This one is in the 33rd percentile – i.e., 33% 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 352,967 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 41st percentile – i.e., 41% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 58 others from the same source and published within six weeks on either side of this one. This one is in the 43rd percentile – i.e., 43% of its contemporaries scored the same or lower than it.