Fig 2: Effects of MASP-1-inhibition in the bleeding model. To investigate the effects of the MASP-1 inhibitor SGMI-1, the signal intensity relative to the first time point was monitored for activated platelets (CD62P) (A) and fibrin (B). A) Both concentrations of SGMI (20.4 µg/ml; n=4 and 40.8ug/ml; n=2) resulted in a reduced increase of the CD62P signal in comparison to the control (n=6). B) Fibrin deposition was reduced in the presence of SGMI-1 (n=3). The area under the curve (C) was measured using GraphPad Prism. (D) SGMI-1 prolonged the bleeding time (n=3). Data are shown as mean with SD, and p-values for differences between groups were determined with ANOVA or t-test (* p = 0.05, ** p = 0.01, *** p = 0.001).

Fig 3: MBL colocalises with activated platelets. Microfluidic bleeding model 60 min after injury. From top left to bottom right: Brightfield, anti-MBL signal (green), anti-CD62P signal (purple), and merged signals. CD62P-expressing activated platelets and MBL showed a complete colocalisation. Scale bar: 50 µm.

Fig 4: Effects of inhibiting MBL-binding in the bleeding model. To investigate the effects of the MBL inhibitory antibody 3F8, the signal intensity relative to the first time point was monitored for MBL (A), MASP-1 (B), activated platelets (CD62P) (C) and fibrin (D). The area under the curve was calculated using GraphPad Prism (E). Experiments using the inhibitory 3F8 antibody showed a reduced increase of the MBL, MASP-1 and CD62P signal in comparison to the non-inhibitory control antibody 1C10, but no clear difference in fibrin signals was detected. Each experiment was performed three times, data are shown as mean with SD, and p-values for differences between groups were determined with a t-test (ns not significant, * p = 0.05, ** p = 0.01, *** p = 0.001).