Abstract：
:Many studies indicate that chronic stress and excessive stress hormone can cause an inflammatory response. Thioredoxin-interacting protein (Txnip) as an endogenous thioredoxin inhibitor suppresses thioredoxin-produced antioxidant effects. Txnip was also found to interact with nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), which activates NLRP3 inflammasome and promotes inflammatory processes. Recently our laboratory found that chronic stress can increase Txnip protein levels in mouse brain, indicating that Txnip may mediate chronic stress-induced inflammation. Microglia play an important role in neuroinflammation. The purpose of this study is to investigate the effect of chronic stress hormone treatment on Txnip and NLRP3 inflammasome signaling in cultured microglia cells. Our result showed that chronic treatment with stress hormone corticosterone increased Txnip protein levels and Txnip-NLRP3 binding in N9 mouse microglia, in primary cultured mouse microglia and in mouse brain. Our result also showed that chronic corticosterone treatment increased procaspase-1 cleavage, caspase-1 activity and interleukin-1β release in N9 microglia. Using CRISPR/Cas9 method we found that knocking out Txnip inhibited corticosterone-increased caspase-1 activity and interleukin-1β release. Our results suggest that chronic corticosterone treatment upregulates Txnip and increases Txnip-NLRP3 binding, which activates NLRP3 inflammasome, resulting in activation of caspase-1 and in further releasing of interleukin-1β. It is therefore likely that Txnip-activated NLRP3 inflammasome contributes to corticosterone-caused neuroinflammation.
journal_name
Neurochem Intjournal_title
Neurochemistry internationalauthors
Bharti V,Tan H,Zhou H,Wang JFdoi
10.1016/j.neuint.2019.104564subject
Has Abstractpub_date
2019-12-01 00:00:00pages
104564eissn
0197-0186issn
1872-9754pii
S0197-0186(19)30262-1journal_volume
131pub_type
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