Laser injury of the perfused endothelial monolayer induces a procoagulant surface by PS exposure and secretion of VWF. (A) Laser pulse to the endothelial monolayer (arrow) perfused with media (at shear 100 s–1), induces an endothelial injury of ∼10 μm with subsequent PS exposure (measured by annexin V binding, red) within 1 minute, but does not disrupt endothelial junctions. Representative images. Scale bar, 20 μm. (B) Laser pulse to the endothelial monolayer (arrow) perfused with media under shear 800 s–1, leads to the secretion of VWF (cyan) from the injured endothelium (stained with annexin V, red). Scale bar, 50 μm. Number of strings counted on annexin V-positive cells (injury, cyan) vs surrounding annexin V-negative cells (gray). Mean ± standard deviation (SD), n = 7 injuries from n = 3 independent experiments, paired t test. DIC, differential interference contrast.
Figure 2.

Laser injury of the perfused endothelial monolayer induces a procoagulant surface by PS exposure and secretion of VWF. (A) Laser pulse to the endothelial monolayer (arrow) perfused with media (at shear 100 s–1), induces an endothelial injury of ∼10 μm with subsequent PS exposure (measured by annexin V binding, red) within 1 minute, but does not disrupt endothelial junctions. Representative images. Scale bar, 20 μm. (B) Laser pulse to the endothelial monolayer (arrow) perfused with media under shear 800 s–1, leads to the secretion of VWF (cyan) from the injured endothelium (stained with annexin V, red). Scale bar, 50 μm. Number of strings counted on annexin V-positive cells (injury, cyan) vs surrounding annexin V-negative cells (gray). Mean ± standard deviation (SD), n = 7 injuries from n = 3 independent experiments, paired t test. DIC, differential interference contrast.

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