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• W2156848575 abstract "Serum amyloid A (SAA) proteins are known to be surrogate markers of sepsis, but their pathogenic roles remain poorly elucidated. Here we provide evidence to support a possible role of SAA as a pathogenic mediator of lethal sepsis. In a subset of septic patients for which serum high mobility group box 1 (HMGB1) levels paralleled the clinical scores, some anti-HMGB1 antibodies detected a 12-kDa protein belonging to the SAA family. In contrast to the most abundant SAA1, human SAA induced double-stranded RNA-activated protein kinase R (PKR) expression and HMGB1 release in the wild-type, but not toll-like receptor 4/receptor for advanced glycation end products (TLR4/RAGE)-deficient, macrophages. Pharmacological inhibition of PKR phosphorylation blocked SAA-induced HMGB1 release, suggesting an important role of PKR in SAA-induced HMGB1 release. In animal models of lethal endotoxemia and sepsis, recombinant SAA exacerbated endotoxemic lethality, whereas SAA-neutralizing immunoglobulins G (IgGs) significantly improved animal survival. Collectively, these findings have suggested SAA as an important mediator of inflammatory diseases. Highlights of this study include: human SAA is possibly only expressed in a subset of septic patients; SAA induces HMGB1 release via TLR4 and RAGE receptors; SAA supplementation worsens the outcome of lethal endotoxemia; whereas SAA-neutralizing antibodies confer protection against lethal endotoxemia and sepsis." @default.
• W2156848575 created "2016-06-24" @default.
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• W2156848575 date "2015-01-01" @default.
• W2156848575 modified "2023-10-18" @default.
• W2156848575 title "Serum Amyloid A Stimulates PKR Expression and HMGB1 Release Possibly through TLR4/RAGE Receptors" @default.
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• W2156848575 cites W1614633287 @default.
• W2156848575 cites W1651940804 @default.
• W2156848575 cites W1946507092 @default.
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• W2156848575 cites W1973404097 @default.
• W2156848575 cites W1973557324 @default.
• W2156848575 cites W1982348992 @default.
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• W2156848575 cites W1990122501 @default.
• W2156848575 cites W1992944558 @default.
• W2156848575 cites W1993034428 @default.
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• W2156848575 cites W2036222920 @default.
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• W2156848575 cites W2075035271 @default.
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• W2156848575 doi "https://doi.org/10.2119/molmed.2015.00109" @default.
• W2156848575 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4607615" @default.
• W2156848575 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26052716" @default.
• W2156848575 hasPublicationYear "2015" @default.
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