ArticleScientific reports2016
Regnase-1 in microglia negatively regulates high mobility group box 1-mediated inflammation and neuronal injury.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Innate immune signalling, neuroinflammation and network plasticity in temporal lobe epilepsy.Frontiers in pharmacology · 2026Review
- The Regnase pathway: a core axis in immune regulation and inflammatory disease.Frontiers in immunology · 2026Review
- Article
- Enrichment of a neutrophil-like monocyte transcriptional state in glioblastoma myeloid suppressor cells.Research square · 2023Article
- The homeostatic function of Regnase-2 restricts neuroinflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Muscone improves hypoxia/reoxygenation (H/R)-induced neuronal injury by blocking HMGB1/TLR4/NF-κB pathwayPeerJ · 2022Article
- Anti-Inflammatory Effects of a Polyphenol, Catechin-7,4'-Pharmaceutics · 2021Article
- Monocyte Chemotactic Protein-Induced Protein 1 (MCPIP-1): A Key Player of Host Defense and Immune Regulation.Frontiers in immunology · 2021Review
- Paeonol attenuates inflammation by targeting HMGB1 through upregulating miR-339-5p.Scientific reports · 2019Article
- Cell permeable HMGB1-binding heptamer peptide ameliorates neurovascular complications associated with thrombolytic therapy in rats with transient ischemic stroke.Journal of neuroinflammation · 2018Article
- MCPIP1-induced autophagy mediates ischemia/reperfusion injury in endothelial cells via HMGB1 and CaSR.Scientific reports · 2018Article
- Omega-3 polyunsaturated fatty acid supplementation attenuates microglial-induced inflammation by inhibiting the HMGB1/TLR4/NF-κB pathway following experimental traumatic brain injury.Journal of neuroinflammation · 2017Article
- Regnase-1, a rapid response ribonuclease regulating inflammation and stress responses.Cellular & molecular immunology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular high mobility group box 1 (HMGB1) has been demonstrated to function as a proinflammatory cytokine and induces neuronal injury in response to various pathological stimuli in central nervous system (CNS). However, the regulatory factor involved in HMGB1-mediated inflammatory signaling is largely unclear. Regulatory RNase 1 (Regnase-1) is a potent anti-inflammation enzyme that can degrade a set of mRNAs encoding proinflammatory cytokines. The present study aims to determine the role of Regnase-1 in the regulation of HMGB1-mediated inflammatory injury in CNS. Cultured microglia and rat brain were treated with recombinant HMGB1 to examine the induction of Regnase-1 expression. Moreover, the role of Regnase-1 in modulating the expression of inflammatory cytokines and neuronal injury was then investigated in microglia by specific siRNA knockdown upon HMGB1 treatment. Results showed that HMGB1 could significantly induce the de novo synthesis of Regnase-1 in cultured microglia. Consistently, Regnase-1 was elevated and found to be co-localized with microglia marker in the brain of rat treated with HMGB1. Silencing Regnase-1 in microglia enhanced HMGB1-induced expression of proinflammatory cytokines and exacerbated neuronal toxicity. Collectively, these results suggest that Regnase-1 can be induced by HMGB1 in microglia and negatively regulates HMGB1-mediated neuroinflammation and neuronal toxicity.
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