Figure 2
Figure 2. Macrophage Flt1 and CNB1 in wound repair. (A) Quantification of ARA vessels in Flt1 control and mutant aortas. (B,C) Immunolabeling for Iba1 (wound macrophages) and Flt1 in control (Wlsfl/fl) and mutant (Wlsfl/fl;cfms-icre) wound sections (B) and quantification of Flt1 staining intensity (C) (×100). (D) Images of wounds in Flt1 control and mutant animals 5 days after initial injury (×20). (E) Quantification of wound size in Flt1 control and mutant animals. (F) Quantitative reverse-transcription polymerase chain reaction for soluble Flt1 from EOC-2 cells exposed for 24 hours to the factors indicated. (G) Time course of wound repair in animals deficient in CNB1. Statistical analysis was performed using one-way analysis of variance with Tukey’s post-hoc test (A, E, F) and Student t test (C, G) using SPSS (IBM, Armonk, NY) software.

Macrophage Flt1 and CNB1 in wound repair. (A) Quantification of ARA vessels in Flt1 control and mutant aortas. (B,C) Immunolabeling for Iba1 (wound macrophages) and Flt1 in control (Wlsfl/fl) and mutant (Wlsfl/fl;cfms-icre) wound sections (B) and quantification of Flt1 staining intensity (C) (×100). (D) Images of wounds in Flt1 control and mutant animals 5 days after initial injury (×20). (E) Quantification of wound size in Flt1 control and mutant animals. (F) Quantitative reverse-transcription polymerase chain reaction for soluble Flt1 from EOC-2 cells exposed for 24 hours to the factors indicated. (G) Time course of wound repair in animals deficient in CNB1. Statistical analysis was performed using one-way analysis of variance with Tukey’s post-hoc test (A, E, F) and Student t test (C, G) using SPSS (IBM, Armonk, NY) software.

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