Figure 4
Figure 4. Histopathologic analysis of the liver, heart and diaphragm in adult mice. (A-D) Livers from A10ΔEC animals had enlarged vessels under the surface in gross (A) and histologic (C) specimens that were not present in livers from control animals (B,D). (E-F) MECA-32 immunohistochemistry of liver sections from A10ΔEC (E) and control (F) individuals showed positive staining for endothelial cells lining vascular structures. Arrows mark the abnormally enlarged vessels in panels A,C and E. (G,H) Liver sections from A10ΔEC mice demonstrated areas of coagulative necrosis (G, arrow) not present in controls (H). (I,J) A heart from an A10ΔEC animal showed numerous, dilated, superficial blood-filled vascular structures (marked by an arrow in panel I) that were not present in a heart from a control animal (J). (K,L) MECA-32 immunohistochemistry of a heart section from an A10ΔEC mouse (K) showed positive staining for endothelial cells surrounding the enlarged vascular structures (pointed by an arrow in panel K) that were not present in a control heart (I). (M-N) Histopathologic analyses of muscular diaphragm specimens revealed increased cellularity between myofibers in A10ΔEC animals (M, arrow) compared with controls (N). (O-P) MECA-32 immunohistochemistry of diaphragm sections from A10ΔEC (O) and control (P) individuals showed positive staining of cells present between myofibers of A10ΔEC diaphragms (arrow in panel O). The micrographs of vascular abnormalities on H&E-stained sections are representative of all animals analyzed for each genotype (n = 6). Scale bars in panels A-B: 1000 μm; C-D: 100 μm; E-H,K-P: 20 μm; I-J: 500 μm.

Histopathologic analysis of the liver, heart and diaphragm in adult mice. (A-D) Livers from A10ΔEC animals had enlarged vessels under the surface in gross (A) and histologic (C) specimens that were not present in livers from control animals (B,D). (E-F) MECA-32 immunohistochemistry of liver sections from A10ΔEC (E) and control (F) individuals showed positive staining for endothelial cells lining vascular structures. Arrows mark the abnormally enlarged vessels in panels A,C and E. (G,H) Liver sections from A10ΔEC mice demonstrated areas of coagulative necrosis (G, arrow) not present in controls (H). (I,J) A heart from an A10ΔEC animal showed numerous, dilated, superficial blood-filled vascular structures (marked by an arrow in panel I) that were not present in a heart from a control animal (J). (K,L) MECA-32 immunohistochemistry of a heart section from an A10ΔEC mouse (K) showed positive staining for endothelial cells surrounding the enlarged vascular structures (pointed by an arrow in panel K) that were not present in a control heart (I). (M-N) Histopathologic analyses of muscular diaphragm specimens revealed increased cellularity between myofibers in A10ΔEC animals (M, arrow) compared with controls (N). (O-P) MECA-32 immunohistochemistry of diaphragm sections from A10ΔEC (O) and control (P) individuals showed positive staining of cells present between myofibers of A10ΔEC diaphragms (arrow in panel O). The micrographs of vascular abnormalities on H&E-stained sections are representative of all animals analyzed for each genotype (n = 6). Scale bars in panels A-B: 1000 μm; C-D: 100 μm; E-H,K-P: 20 μm; I-J: 500 μm.

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