Fig. 4

HMGB1 increased GEnC activation and injury in the presence of patient-derived MPO-ANCA-positive IgGs through moesin. Levels of both sICAM-1 and sVCAM-1 increased significantly in the supernatants of GEnCs treated with HMGB1 plus patient-derived MPO-ANCA-positive IgGs compared with untreated cells, cells treated with HMGB1 or patient-derived MPO-ANCA-positive IgGs alone (a, b). Levels of LDH release increased significantly in the supernatants of GEnCs treated with HMGB1 plus patient-derived MPO-ANCA-positive IgGs compared with untreated cells, cells treated with HMGB1 or patient-derived MPO-ANCA-positive IgGs alone (c). Levels of vascular barrier disruption increased significantly in GEnCs treated with HMGB1 plus patient-derived MPO-ANCA-positive IgGs compared with untreated cells, cells treated with HMGB1 or patient-derived MPO-ANCA-positive IgGs alone (d). By preincubating with anti-moesin antibodies, levels of cell activation, LDH release and levels of vascular barrier disruption decreased significantly (a–d). Bars represent mean ± SD of repeated measurements from five independent experiments. Ab antibody, ANCA antineutrophil cytoplasmic antibody, GEnC glomerular endothelial cell, HMGB1 high mobility group box-1, LDH lactate dehydrogenase, MPO myeloperoxidase, OD optical density, sICAM-1, soluble intercellular cell adhesion molecule-1, sVCAM-1, soluble vascular cell adhesion molecule-1