Data Management And Sharing System of China National Clinical Research Center for Neurological Diseases
Extracellular ASC exacerbated the recurrent ischemic stroke in an NLRP3-dependent manner
First author：He Xiao-Fei
Corresponding author：Pei Zhong
essential_information
- Person in charge：He Xiao-Fei
- Data Sources： OTHERS
- Number of papers：OTHERS20190781
- Published time：2019-06-19
2019-06-19
Published articles
Journal：Journal of cerebral blood flow and metabolism
Publication type: Original Article
IF(IF): 6.2
PMID: 31216943 Link To Pubmed Full text Download
Background And Purpose
Method
Next, using a photothrombotic mouse model of recurrent stroke, we found that recurrent strokes increased the activation of NLRP3, exacerbated the brain damage and the pro-inflammatory response in wild type (WT) mice, but not in NLRP3 knockout (NLRP3 KO) mice.
Conclusion
We therefore conclude that the NLRP3 inflammasome is activated by two attacks of stroke, which act together with ASC to exacerbate recurrent strokes.
Main results
Additionally, we found that apoptosis-associated speck-like protein containing a CARD (ASC) protein level surrounding the infarct area was comparatively increased, but that ASC specks outside of microglia in both the ipsilateral and contralateral of stroke site were decreased in NLRP3 KO mice relative to wild-type (WT) controls, and the number of ASC specks surrounding the second infarct area was positively correlated to the damage scores. Mechanistically, we found that recombinant ASC (RecASC) activated NLRP3 and induced pro-inflammatory responses, exacerbating the outcome of ischemic stroke, in WT mice, but not in NLRP3 KOmice.