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Image Search Results
Journal: Molecular immunology
Article Title: Complement activation on neutrophils initiates endothelial adhesion and extravasation
doi: 10.1016/j.molimm.2019.09.011
Figure Lengend Snippet: In vitro C5a-induced degranulated neutrophil contents degrade VE-cadherin, generating intercellular gaps. A) C5a-induced degranulated neutrophil contents (30 ng of supernatant) were incubated with HUVEC monolayers. Loss of VE-cadherin (asterisks, left lower panel) and appearance of intercellular gaps (right lower panel) at time 0 (Media) and 30 min. VE-cadherin (red), F-actin (green), DAPI (blue). Scale bar = 30 μm. B) Quantification of intercellular gap formation over time, as detailed in Methods. C) Incubation of C5a-induced degranulated neutrophil supernatant with HUVECs led to VE-cadherin degradation. D) Neutrophil protease inhibitors, specifically NE inhibitor (NEi) or the combination of CGi, NEi, PR3i and MMPi (x4i), blocked VE-cadherin degradation. Actin served as control for protein loading. Statistical analysis was performed using one-way ANOVA.
Article Snippet: For immunofluorescence the chamber slides were blocked with 0.3% Triton X-100 (Thermo Fisher Scientific, Waltham, MA) with the addition of 10% goat serum (Sigma, Saint Louis MO) for 1 h at RT followed by incubation with
Techniques: In Vitro, Incubation