Fig. 5: EPRS1 negatively regulates inflammation in TLR-stimulated macrophages.
From: Glutamyl-prolyl-tRNA synthetase 1 coordinates early endosomal anti-inflammatory AKT signaling
a Immunoblot analysis of phosphorylated- and total EPRS1, AKT, GSK3β, CREB, and NF-kB p65, and of actin, in LPS-treated BMDMs isolated from Eprs1fl/fl and Eprs1fl/flLyz2Cre mice. b Immunoblot analysis of cell lysates from LPS-treated RAW 264.7 cells transfected with EPRS1-specific siRNA (siEPRS1) or control (non-targeting) siRNA (siCon) using the indicated antibodies. c–e Enzyme-linked immunosorbent assay of TNF-α (c), IL-6 (d), and IL-10 (e) in supernatants from BMDMs isolated from Eprs1fl/fl and Eprs1fl/flLyz2Cre mice stimulated for 24 h with TLR ligands (BLP, 100 ng/ml; ZYM, 10 μg/ml; poly(I:C), 40 μg/ml; LPS, 100 ng/ml, and CpG, 1 μg/ml). f–h Concentration of TNF-α (f), IL-6 (g), and IL-10 (h) in supernatants from peritoneal macrophages isolated from Eprs1fl/fl and Eprs1fl/flLyz2Cre mice stimulated with LPS (100 ng/ml) for 12 or 24 h, as quantified by ELISA. i–k Concentrations of TNF-α (i), IL-6 (j), and IL-10 (k) in supernatants from RAW 264.7 cells transfected with siCon or siEPRS1, followed by stimulation with LPS (100 ng/ml) for the indicated times. The data shown are representative of three independent experiments, each with similar results. Data are expressed as the mean ± SEM. Two-tailed unpaired t-tests were used. Source data are provided as a Source Data file.
