Extracellular CIRP (eCIRP) and inflammation

Cold‐inducible RNA‐binding protein (CIRP) was discovered 2 decades ago while studying the mechanism of cold stress adaptation in mammals. Since then, the role of intracellular CIRP (iCIRP) as a stress‐response protein has been extensively studied. Recently, extracellular CIRP (eCIRP) was discovered...

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Vydáno v:	Journal of leukocyte biology Ročník 106; číslo 1; s. 133 - 146
Hlavní autoři:	Aziz, Monowar, Brenner, Max, Wang, Ping
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	England Oxford University Press 01.07.2019
Témata:	Alarmins - physiology ALI Animals CIRP Cytosol Damage patterns DAMP Dendritic cells DNA damage eCIRP Endoplasmic reticulum Endoplasmic Reticulum Stress Endothelial cells hemorrhage Humans Inflammasomes Inflammation Inflammation - drug therapy Inflammation - etiology Inflammation Mediators - physiology Inflammatory diseases Ischemia ischemia/reperfusion Leukocytes (neutrophilic) Lymphocytes macrophage Macrophages Mitochondrial DNA Necroptosis neutrophils Neutrophils - physiology NF-κB protein Proteins Pyroptosis Reperfusion RNA-binding protein RNA-Binding Proteins - antagonists & inhibitors RNA-Binding Proteins - physiology Sepsis Signal Transduction Therapeutic applications Therapeutic targets TLR4 protein Toll-Like Receptor 4 - physiology Toll-like receptors Translocation ischemia/reperfusion inflammation eCIRP macrophage CIRP neutrophils ALI sepsis DAMP hemorrhage
ISSN:	0741-5400, 1938-3673, 1938-3673
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Popis
Shrnutí:	Cold‐inducible RNA‐binding protein (CIRP) was discovered 2 decades ago while studying the mechanism of cold stress adaptation in mammals. Since then, the role of intracellular CIRP (iCIRP) as a stress‐response protein has been extensively studied. Recently, extracellular CIRP (eCIRP) was discovered to also have an important role, acting as a damage‐associated molecular pattern, raising critical implications for the pathobiology of inflammatory diseases. During hemorrhagic shock and sepsis, inflammation triggers the translocation of CIRP from the nucleus to the cytosol and its release to the extracellular space. eCIRP then induces inflammatory responses in macrophages, neutrophils, lymphocytes, and dendritic cells. eCIRP also induces endoplasmic reticulum stress and pyroptosis in endothelial cells by activating the NF‐κB and inflammasome pathways, and necroptosis in macrophages via mitochondrial DNA damage. eCIRP works through the TLR4‐MD2 receptors. Studies with CIRP−/− mice reveal protection against inflammation, implicating eCIRP to be a novel drug target. Anti‐CIRP Ab or CIRP‐derived small peptide may have effective therapeutic potentials in sepsis, acute lung injury, and organ ischemia/reperfusion injuries. The current review focuses on the pathobiology of eCIRP by emphasizing on signal transduction machineries, leading to discovering novel therapeutic interventions targeting eCIRP in various inflammatory diseases. Review on the pathobiology, signal transduction and novel therapeutic strategies involving eCIRP in inflammatory diseases.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23 PW discovered eCIRP and conceived the idea of the project. MA compiled literature review. MA, MB, PW outlined the concept of the review. MA, MB wrote the manuscript and prepared the figures and table. PW reviewed, provided constructive criticism and edited the manuscript. PW supervised the study. Authorship
ISSN:	0741-5400 1938-3673 1938-3673
DOI:	10.1002/JLB.3MIR1118-443R