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Results: 7

1.
Figure 6

Figure 6. From: Contributions of extravascular and intravascular cells to fibrin network formation, structure, and stability.

Fibrin network density correlates with cellular expression of TF activity. Factor Xa generation (○, A), prothrombinase activity (●, B), and fibrin density (x-axis) were measured in reactions with HUVECs, SMCs, TNFα-stimulated HUVECs, and fibroblasts (left to right) as described in “TF, prothrombinase activity, and activated protein C generation assays.”

Robert A. Campbell, et al. Blood. 2009 November 26;114(23):4886-4896.
2.
Figure 5

Figure 5. From: Contributions of extravascular and intravascular cells to fibrin network formation, structure, and stability.

In situ thrombin generation influences clot stability. Clots were formed by incubating cells with recalcified normal, pooled PFP in the presence of tPA (250 ng/mL) and clot formation and lysis were monitored by an increase and subsequent decrease in turbidity at 405 nm. All values for (A) time to peak and (B) peak turbidity (± SD) were statistically different (*P < .05) compared with HUVECs.

Robert A. Campbell, et al. Blood. 2009 November 26;114(23):4886-4896.
3.
Figure 3

Figure 3. From: Contributions of extravascular and intravascular cells to fibrin network formation, structure, and stability.

β 3 integrins do not modulate fibrin structure on fibroblasts, SMCs, or HUVECs. In situ thrombin generation was initiated by incubating fibroblasts, SMCs, and HUVECs with recalcified, normal, pooled PFP in the presence of 0.136μM control IgG or anti-β3 antibody (abciximab) as described in “Methods.” Three-dimensional projections show clot architecture in 10-μm stacks 0 to 10 μm from the cell surface. Each image (146 μm × 146 μm, xy) is from 1 experiment, representative of 2 to 5 separate experiments. Data (no. fibers/point, ± SD) indicate mean fibrin network density from all experiments. Fibrin density in clots formed in the presence of control IgG or abciximab was not statistically different.

Robert A. Campbell, et al. Blood. 2009 November 26;114(23):4886-4896.
4.
Figure 4

Figure 4. From: Contributions of extravascular and intravascular cells to fibrin network formation, structure, and stability.

β 3 integrins modulate fibrin structure on platelets. (A,C) Clotting was initiated on platelets with the addition of recalcified, normal, pooled PFP to lipidated TF (1:120 000, final), in the presence of 0.136μM control IgG (A) or the anti-b3 Fab abciximab (C). (B,D) Clotting was initiated on platelets with the addition of fibrinogen, calcium, and thrombin (2 mg/mL, 5mM, and 2nM, respectively), in the presence of 0.136μM control IgG (B) or abciximab (D). Three-dimensional projections (146 μm × 146 μm, xy) show clot architecture in 10-μm stacks at 0 to 10 μm from the cell surface. Each image is from 1 experiment, representative of 4 independent experiments. Darker areas show increased fibrin density. Arrows in panels A and B indicate increased fibrin density surrounding individual platelets. (E) Data (± SD) indicate mean fibrin network density from all experiments. *P < .004 versus corresponding control IgG

Robert A. Campbell, et al. Blood. 2009 November 26;114(23):4886-4896.
5.
Figure 1

Figure 1. From: Contributions of extravascular and intravascular cells to fibrin network formation, structure, and stability.

Extravascular and intravascular cells support different levels of thrombin generation and fibrin formation. Recalcified (10mM, final) normal, pooled PFP was added to confluent cell monolayers. (A) Thrombin generation was measured using calibrated automated thrombography; data (± SD) shown are averaged from at least 5 separate experiments. (A inset) HUVECs were incubated with TNFα (0-1nM) for 4 hours at 37°C. Factor Xa generation (± SD) was measured by incubating cells with factors VIIa and X in the presence of CaCl2, and measuring factor Xa generation by chromogenic substrate in 2 separate experiments. (B) Fibrin polymerization was measured by turbidity at 405 nm; data (± SD) shown are from 1 experiment, representative of at least 7 independent experiments. Symbols for panels A and B are as follows: fibroblasts, (●); SMCs, (♦); HUVECs, (■); and HUVECs stimulated with TNFα for 4 hours, (▴).

Robert A. Campbell, et al. Blood. 2009 November 26;114(23):4886-4896.
6.
Figure 2

Figure 2. From: Contributions of extravascular and intravascular cells to fibrin network formation, structure, and stability.

In situ thrombin generation on the cell surface modulates clot architecture in 3 dimensions. Clots were formed by incubating cells with recalcified normal, pooled PFP in the presence of 500μM (final) control peptide GRGESP (A-H) or GRGDSP (I-L). Three-dimensional projections show clot architecture in 10-μm stacks at (E-L) and above (A-D) the cell surface. Each image (146 μm × 146 μm, xy) is from 1 experiment, representative of at least 3 independent experiments. Darker areas show increased fibrin density. (M) Fibrin network density (± SD) of clots produced by fibroblasts (●), SMCs (♦), HUVECs (■), and TNFα-stimulated HUVECs (▴) was determined as described in “Methods” from at least 3 independent experiments. (N) Clots were formed in excised human saphenous vein segments as described in “Structural analysis of ex vivo clots by transmission electron microscopy.” Clots were then fixed, examined by transmission electron microscopy, and fibrin fibers (black dots) were quantified at (0 μm) and above (5 μm) from the cell surface (indicated by black rectangles). Original magnification, × 2000; bar represents 5 μm. The image is representative of 3 independent experiments.

Robert A. Campbell, et al. Blood. 2009 November 26;114(23):4886-4896.
7.
Figure 7

Figure 7. From: Contributions of extravascular and intravascular cells to fibrin network formation, structure, and stability.

TF inhibition prolongs the onset and reduces the rate of thrombin generation and clot formation, resulting in a less dense fibrin network. Recalcified (10mM, final) normal pooled PFP was added to confluent HUVECs and TNFα-treated HUVEC monolayers in the presence of anti-TF antibody (10 μg/mL anti–human TF antibody) or IgG control. (A) Thrombin generation was measured by calibrated automated thrombography. Data (± SD) show the average of 5 separate experiments. (B) Fibrin polymerization was monitored by turbidity at 405 nm. Data (± SD) shown are from 1 experiment, representative of 4 separate experiments. Symbols for panels A and B are HUVECs plus: IgG, (■); anti-TF, (□); TNFα+IgG, (▴); TNFα+anti-TF, (▵). (C) Three-dimensional projections (146 μm × 146 μm, xy) show clot architecture in 10-μm stacks 0 to 10 μm from the surface of unstimulated or TNFα-stimulated HUVECs in the presence or absence of anti-TF, as indicated. Each image is from 1 experiment, representative of 4 independent experiments. (D) Fibrin density (± SD) was measured as described in “Methods.” (E-F) Clotting was initiated in the presence of tPA (250 ng/mL) and the time to peak and peak turbidity were calculated from resulting turbidity curves. Data (± SD) show the average of 9 independent experiments. *P < .05 versus unstimulated HUVECs.

Robert A. Campbell, et al. Blood. 2009 November 26;114(23):4886-4896.

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