Figure 4.
Figure 4. Eap inhibits neovascularization in wound healing. (A) Typical photomicrographs (× 100 magnification) of immunohistochemical staining for the detection of PECAM-1 (CD31) in association with blood vessels at day 5 following wound generation in the absence (buffer) or presence of 20 μg Eap is shown. Negative control (first antibody omitted) is also shown. (B) Statistical evaluation of the density of CD31-positive blood vessels (expressed as number of vessels/field) in wound sections at day 5 following wound generation in the absence (buffer) or presence of 20 μg Eap is shown. Evaluation of 7 fields per wound from 8 wounds per treatment group is shown. (C) Mice were anesthetized and fluorescent microbeads were injected. The recovered fluorescence per weight of wound tissue is shown, and data expressed relative to control (buffer-treated wounds) are means ± SD of 10 wounds. *P < .01 compared with control.

Eap inhibits neovascularization in wound healing. (A) Typical photomicrographs (× 100 magnification) of immunohistochemical staining for the detection of PECAM-1 (CD31) in association with blood vessels at day 5 following wound generation in the absence (buffer) or presence of 20 μg Eap is shown. Negative control (first antibody omitted) is also shown. (B) Statistical evaluation of the density of CD31-positive blood vessels (expressed as number of vessels/field) in wound sections at day 5 following wound generation in the absence (buffer) or presence of 20 μg Eap is shown. Evaluation of 7 fields per wound from 8 wounds per treatment group is shown. (C) Mice were anesthetized and fluorescent microbeads were injected. The recovered fluorescence per weight of wound tissue is shown, and data expressed relative to control (buffer-treated wounds) are means ± SD of 10 wounds. *P < .01 compared with control.

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