Figure 6
Figure 6. Decreased neovascularization in the wound area of CSF-1op/op mice. (A) Representative macroscopic views of full-thickness excisional wounds in the back skin of CSF-1+/+ or CSF-1op/op mice. Note delayed wound closure in CSF-1op/op mice. (B) Percentage of wound closure of dorsal excisional wounds (n = 6). (C-L) Hematoxylin and eosin staining (C-D) or immunohistochemistry of Keratin5 (green), α-smooth muscle actin (red), and 4,6-diamidino-2-phenylindole (blue) (E-L) in the healing edges at 7 days after wounding. Note delayed epidermal closure (E-F) and dermal contraction (G-H) in CSF-1op/op mice (asterisks). (M-N) Immunohistochemistry of F4/80 (green) and 4,6-diamidino-2-phenylindole (blue) in the healing edges at 7 days after wounding. Macrophages are abundantly recruited in the healing edge of CSF-1+/+ (arrowheads) but not in that of CSF-1op/op mice. (O-P) Representative macroscopic views of the ventral sides of the dorsal excisional wounds in CSF-1+/+ or CSF-1op/op mice (7 days after wounding). Note decreased vessels in the wound area of CSF-1op/op mice. (Q-R) Images for sectional immunohistochemistry of CD31. Neovascularization is decreased in the wound area of CSF-1op/op mice compared with that of CSF-1+/+ mice. (S-T) Quantification in the capillary density or the number of BrdU+ cells in the healing edges 7 days after wounding (n = 6). (U) Representative Western blotting for the wound tissues at 7 days after wounding. Although VEGF expression was not altered, MMP-9 and MMP-2 were down-regulated in CSF-1op/op mice. Bars represent 5 mm in A; 500 μm in C-L,O-P; and 50 μm in M-N,Q-R. *P < .05. **P < .01.

Decreased neovascularization in the wound area of CSF-1op/op mice. (A) Representative macroscopic views of full-thickness excisional wounds in the back skin of CSF-1+/+ or CSF-1op/op mice. Note delayed wound closure in CSF-1op/op mice. (B) Percentage of wound closure of dorsal excisional wounds (n = 6). (C-L) Hematoxylin and eosin staining (C-D) or immunohistochemistry of Keratin5 (green), α-smooth muscle actin (red), and 4,6-diamidino-2-phenylindole (blue) (E-L) in the healing edges at 7 days after wounding. Note delayed epidermal closure (E-F) and dermal contraction (G-H) in CSF-1op/op mice (asterisks). (M-N) Immunohistochemistry of F4/80 (green) and 4,6-diamidino-2-phenylindole (blue) in the healing edges at 7 days after wounding. Macrophages are abundantly recruited in the healing edge of CSF-1+/+ (arrowheads) but not in that of CSF-1op/op mice. (O-P) Representative macroscopic views of the ventral sides of the dorsal excisional wounds in CSF-1+/+ or CSF-1op/op mice (7 days after wounding). Note decreased vessels in the wound area of CSF-1op/op mice. (Q-R) Images for sectional immunohistochemistry of CD31. Neovascularization is decreased in the wound area of CSF-1op/op mice compared with that of CSF-1+/+ mice. (S-T) Quantification in the capillary density or the number of BrdU+ cells in the healing edges 7 days after wounding (n = 6). (U) Representative Western blotting for the wound tissues at 7 days after wounding. Although VEGF expression was not altered, MMP-9 and MMP-2 were down-regulated in CSF-1op/op mice. Bars represent 5 mm in A; 500 μm in C-L,O-P; and 50 μm in M-N,Q-R. *P < .05. **P < .01.

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