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- W1429506543 abstract "Neutrophils are critical mediators of the innate immune response that capture and kill invading pathogens. Key to this activity is production of neutrophil extracellular traps, DNA-based structures extruded by neutrophils to capture and kill invading microbes. The identification of G protein-coupled receptors (GPCRs) that can either enhance or inhibit NET production may facilitate the development of novel therapeutic agents for the treatment of infection and inflammation. Here, we investigated the role of the G protein-coupled estrogen receptor (GPER), recently shown to play a role in innate immune function. Quantitative PCR revealed that GPER is highly expressed in human neutrophils isolated from healthy male and female donors. Fluorescent quantification of extracellular DNA using PicoGreen revealed that both selective (G-36) and general (raloxifene) antagonists of GPER, but not selective antagonists for the nuclear estrogen receptors ERα (MPP) or ERβ (PHTPP) inhibited PMA-induced NET production in human neutrophils. These results were verified using high throughput imaging of fixed, SytoxGreen-stained neutrophils. The activity of GPER antagonists appeared to be independent of Erk1/2 signaling and generation of reactive oxygen species (ROS), pathways known to be critical mediators of NET production. Our data suggest that GPER may be a novel therapeutic target for pharmacological modulation of NET production and potentially for anti-microbial activity." @default.
- W1429506543 created "2016-06-24" @default.
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- W1429506543 date "2015-04-01" @default.
- W1429506543 modified "2023-09-27" @default.
- W1429506543 title "The G protein‐coupled estrogen receptor GPR30 controls immune function by regulating neutrophil extracellular trap formation" @default.
- W1429506543 doi "https://doi.org/10.1096/fasebj.29.1_supplement.772.16" @default.
- W1429506543 hasPublicationYear "2015" @default.
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