Fig. 7

vWF, ICAM-1 and P-Sel participation in endotoxin-induced platelet and neutrophil adhesion to endothelial cells and TRPM7 α-kinase domain participation in endotoxin-induced vWF, ICAM-1 and P-Sel expression. A–F Vehicle- and endotoxin-treated ECs in the presence or absence of the vWF inhibitor Caplacizumab (A, B), the ICAM-1 inhibitor A-286982 and A-205804 (C, D), or the P-Sel inhibitor KF38789 (E, F) and then cocultured with platelets (A, C and E) or neutrophils (B, D and F) for 24 h. or 30 min. respectively, and platelets and neutrophils adhesion was analyzed (N = 3–4). (G–I) Protein expression quantification of vWF (G), ICAM-1 (H) and P-Sel (I) by densitometric analysis from immunofluorescence experiments in vehicle- and endotoxin-treated ECs in the presence or absence of the TRPM7 α-kinase function inhibitor TG100-115 (N = 3–4). Results were normalized against vehicle-treated cells in the absence of inhibitors (control condition). Statistical differences were assessed by a two-way analysis of variance (ANOVA) followed by Tukey post hoc test. ***p < 0.001 and ****p < 0.0001, compared with the vehicle-treated cells in the absence of inhibitors. Results showed as mean ± SEM