Fig. 4: HCAEC activation by NMVs.
From: Neutrophil microvesicles drive atherosclerosis by delivering miR-155 to atheroprone endothelium

HCAEC were cultured for 72 h under static conditions (a) or oscillatory shear stress (OSS; b) and were then incubated with (+NMV) or without (−NMV) NMVs for 2 h (a; n = 5) and 4 h (a; n = 7, b; n = 4). Release of CCL2, CXCL8 and IL-6 into the media was analysed using cytometric bead array (a) or ELISA (b). c HCAEC were incubated with (+NMV) or without (−NMV) NMVs for 2 h under static conditions and alterations in inflammatory protein (n = 5) expression were investigated using western blotting. Samples were quantified using densitometry and normalised to GAPDH. d, e HCAEC were incubated with (+NMV) or without (−NMV) NMVs for 2 h under static conditions (n = 10; upper panel) or OSS (n = 3; lower panel) and gene expression changes measured using RT-qPCR. Samples were normalised to β-actin. Results are presented as mean ± SEM and statistical significance evaluated using a paired t-test. NS not statistically significant, *P < 0.05, **P < 0.01, ***P < 0.001. All n numbers represent independent experiments. Source data are provided as a Source Data file.