Figure 4
Figure 4. Both cellular PCA and the fibrinogen level modulate fibrin network density. (A-B) Clots were formed by incubating unstimulated HSVECs, SMCs, and TNF-α–stimulated HSVEC monolayers with recalcified human NPP spiked with human fibrinogen or BSA, as indicated, and imaged by laser scanning confocal microscopy as described.18,19 (A) Representative micrographs (146 × 146 μm, xy) show 3-dimensional projections from 10-μm stacks at the cell surface (n ≥ 3). Darker areas represent increased fibrin density. (B) Fibrin network density (mean ± SD) of clots was determined as described in “Laser scanning confocal microscopy.” *P < .05 versus 3 mg/mL fibrinogen on HSVECs. #P < .05 versus 3 mg/mL within each cell type. (C) Clots were formed by addition of TF (1:30 000 Innovin) to recalcified murine PPP spiked with human fibrinogen or HBS.

Both cellular PCA and the fibrinogen level modulate fibrin network density. (A-B) Clots were formed by incubating unstimulated HSVECs, SMCs, and TNF-α–stimulated HSVEC monolayers with recalcified human NPP spiked with human fibrinogen or BSA, as indicated, and imaged by laser scanning confocal microscopy as described.18,19  (A) Representative micrographs (146 × 146 μm, xy) show 3-dimensional projections from 10-μm stacks at the cell surface (n ≥ 3). Darker areas represent increased fibrin density. (B) Fibrin network density (mean ± SD) of clots was determined as described in “Laser scanning confocal microscopy.” *P < .05 versus 3 mg/mL fibrinogen on HSVECs. #P < .05 versus 3 mg/mL within each cell type. (C) Clots were formed by addition of TF (1:30 000 Innovin) to recalcified murine PPP spiked with human fibrinogen or HBS.

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