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• W2140341966 startingPage "1796" @default.
• W2140341966 abstract "Abstract The inflammatory response is integral to maintaining health by functioning to resist microbial infection and repair tissue damage. Large numbers of neutrophils are recruited to inflammatory sites to neutralize invading bacteria through phagocytosis and the release of proteases and reactive oxygen species into the extracellular environment. Removal of the original inflammatory stimulus must be accompanied by resolution of the inflammatory response, including neutrophil clearance, to prevent inadvertent tissue damage. Neutrophil apoptosis and its temporary inhibition by survival signals provides a target for anti-inflammatory therapeutics, making it essential to better understand this process. GM-CSF, a neutrophil survival factor, causes a significant increase in mRNA levels for the known anti-apoptotic protein serum and glucocorticoid–regulated kinase 1 (SGK1). We have characterized the expression patterns and regulation of SGK family members in human neutrophils and shown that inhibition of SGK activity completely abrogates the antiapoptotic effect of GM-CSF. Using a transgenic zebrafish model, we have disrupted sgk1 gene function and shown this specifically delays inflammation resolution, without altering neutrophil recruitment to inflammatory sites in vivo. These data suggest SGK1 plays a key role in regulating neutrophil survival signaling and thus may prove a valuable therapeutic target for the treatment of inflammatory disease." @default.
• W2140341966 created "2016-06-24" @default.
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• W2140341966 date "2014-02-15" @default.
• W2140341966 modified "2023-09-27" @default.
• W2140341966 title "Serum and Glucocorticoid–Regulated Kinase 1 Regulates Neutrophil Clearance during Inflammation Resolution" @default.
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• W2140341966 doi "https://doi.org/10.4049/jimmunol.1300087" @default.
• W2140341966 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3921102" @default.
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• W2140341966 hasPublicationYear "2014" @default.
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