Fig 1: MBL and fibrin accumulate upon vessel injury. Microfluidic bleeding model 20 min after injury. From top left to bottom right: Brightfield, anti-MBL signal (green), AlexaFluor647-conjugated fibrin signal (cyan), and merged signals. MBL accumulates at the injury site in a wall-like structure but shows only partial colocalisation with fibrin. Scale bar: 50 µm.
Fig 2: 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 3: 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).
Fig 4: MBL colocalises with von Willebrand factor. Microfluidic bleeding model 45 min after injury. From top left to bottom right: Brightfield, anti-MBL signal (green), anti-von Willebrand factor signal (yellow), and merged signals. MBL and von Willebrand factor showed strong colocalisation. Scale bar: 50 µm.
Supplier Page from Abcam for Anti-Mannan Binding Lectin/MBL antibody