Additional file 1 of Silica nanomaterials induce organ injuries by Ca2+-ROS-initiated disruption of the endothelial barrier and triggering intravascular coagulation

Additional file 1: Figure S1. Blank control (without cell) (a) and positive control (high K+) (b) of the NMT experiments in HUVECs in vitro. Adding SiNPs to the dish solution did not yield obvious biological Ca2+ flux signal but a small mechanical disturb signal was seen in the blank control experiment (a). High K+ (60 mmol/L) induced transient Ca2+ influx in a HUVEC by depolarization (b). Figure S2. Transport rates for silica nanoparticles in vitro. The deposition fractions of SiNP-20 and SiNP-100 were calculated using the ISDD model after delivering these nanoparticles to cell culture medium over a duration of 24 h. Note that the deposition fraction of SiNP-100 was higher than SiNP-20 after exposure for ≥15 h. Parameters included the hydrodynamic diameter measured by DLS, medium column height (3.1 mm), temperature (310 K), medium density (1.00 g/cm3), and medium dynamic viscosity (0.00074 Pa·s). Figure S3. H&E stains of multiple organ tissues showing the toxic effects of SiNP-20 and SiNP-100 at lower doses (7 and 21 mg/kg, i.v.) and exposure for 72 h in mice in vivo. Scal bar = 100 μm for all subpanels. Figure S4. Immunohistochemical stains of F4/80 (macrophage marker, brown) in several organ tissues in vivo which reflect macrophage infiltration in response to lower doses of SiNPs (7 and 21 mg/kg, i.v.). Both SiNPs at 7 mg/kg almost did not induce macrophage infiltration, while at 21 mg/kg induced substantial macrophage infiltration. Scal bar = 50 μm. Figure S5. Confocal images of organ tissues showing the effects of lower doses of SiNP-20 and SiNP-100 (7 and 21 mg/kg, i.v.) on the expression and spatial distribution of VE-cadherin (green) in multiple organ tissues in vivo. Scale bar = 100 μm.