Figure 5
Figure 5. Confocal microscopy of fibrin polymerization. Platelet-poor plasma isolated from control (left panels) and STAT5-deficient (right panels) mice was supplemented with 80 μg/mL human fibrinogen labeled with AlexaFluor 488. Thrombin-triggered clotting was initiated in the center of a 35-mm glass-bottomed dish, and polymerization was recorded at 37°C using a Nikon Ti inverted microscope, 100×/1.49 Apo TIRF objective, Yokogowa CSU-X1 spinning disk confocal unit with 486 nm DPSS laser source, and a Photometrics Cascade II 512 camera. Images are maximum intensity projections of 5-μm stacks at the indicated time points. No discernable fibers were present at the beginning of capture (A-B). Fibrin fibrils first appeared at 120 seconds in STAT5-deficient plasma (C-D) and 180 seconds in control plasma (E-F). At 460 seconds, both control and STAT5-deficient plasma had established extensive fibrin networks (G-H).

Confocal microscopy of fibrin polymerization. Platelet-poor plasma isolated from control (left panels) and STAT5-deficient (right panels) mice was supplemented with 80 μg/mL human fibrinogen labeled with AlexaFluor 488. Thrombin-triggered clotting was initiated in the center of a 35-mm glass-bottomed dish, and polymerization was recorded at 37°C using a Nikon Ti inverted microscope, 100×/1.49 Apo TIRF objective, Yokogowa CSU-X1 spinning disk confocal unit with 486 nm DPSS laser source, and a Photometrics Cascade II 512 camera. Images are maximum intensity projections of 5-μm stacks at the indicated time points. No discernable fibers were present at the beginning of capture (A-B). Fibrin fibrils first appeared at 120 seconds in STAT5-deficient plasma (C-D) and 180 seconds in control plasma (E-F). At 460 seconds, both control and STAT5-deficient plasma had established extensive fibrin networks (G-H).

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