Figure 3
Figure 3. Evaluation of cardiac fibrosis and bleeding in TF-deficient mice. (A-F) Masson trichrome staining of 10-week hearts from TFflox/flox (A,C) and TFflox/flox/SM22αCre+/− (B,D-F) mice. (A,B) Low-power (1.25×/0.04 PlanAPO) cross sections taken midway through the left ventricle. (C,D) Higher-power (40×/0.30 UPlanFL) sections from the same hearts. (E,F) Further magnifications (40×/0.30 UPlanFL) from panel B showing hemosiderin (arrows) and active hemorrhage (red blood cells). Fibrosis appears as blue. (G,H) Prussian blue (Perls Ferric Iron) staining (40×/0.30 UPlanFL) of TFflox/flox (G) and TFflox/flox/SM22αCre+/− (H) mice.

Evaluation of cardiac fibrosis and bleeding in TF-deficient mice. (A-F) Masson trichrome staining of 10-week hearts from TFflox/flox (A,C) and TFflox/flox/SM22αCre+/− (B,D-F) mice. (A,B) Low-power (1.25×/0.04 PlanAPO) cross sections taken midway through the left ventricle. (C,D) Higher-power (40×/0.30 UPlanFL) sections from the same hearts. (E,F) Further magnifications (40×/0.30 UPlanFL) from panel B showing hemosiderin (arrows) and active hemorrhage (red blood cells). Fibrosis appears as blue. (G,H) Prussian blue (Perls Ferric Iron) staining (40×/0.30 UPlanFL) of TFflox/flox (G) and TFflox/flox/SM22αCre+/− (H) mice.

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