FIG. 4.

Regenerative effects of Wnt3a/β-catenin signaling during the chronic phase after traumatic brain injury (TBI). (A-E) At 14 days post-TBI, western blot analysis was performed using peri-contusion tissue from animals given a 7-day treatment regimen. (B) Quantification of the normalized intensity of Wnt3a. (C) Quantification of the normalized intensity of β-catenin. (D) Quantification of the normalized intensity of glial-derived growth factor (GDNF). (E) Quantification of the normalized intensity of vascular endothelial growth factor (VEGF). *p < 0.05. n = 3 for Sham group, n = 9 for both TBI+Saline and TBI+Wnt3a groups. (F-I) Mice received intraperitoneal (i.p.) injections of BrdU starting at 3 days post-TBI and continuing until sacrifice at 14 days post-TBI. (F) Immunohistochemical examination (green: NeuN, red: BrdU:, blue: GLUT1) of the cortical region surrounding the injury site shows that Wnt3a treatment resulted in higher levels of total BrdU+ cells, BrdU+/NeuN+ co-labeled cells (arrow), and BrdU+/GLUT1+ co-labeled cells (arrowheads). (G-I) Distinct subtypes of proliferating cells were quantified and analyzed. Wnt3a treatment resulted in significantly greater levels of overall proliferation (total BrdU+ cells), neurogenesis (BrdU+/NeuN+ co-labeled cells), and angiogenesis (BrdU+/GLUT1+ co-labeled cells) following TBI. *p < 0.05, **p < 0.01. n = 3 for Sham group, n = 6 for both TBI+Saline and TBI+Wnt3a groups. Color image is available online at www.liebertpub.com/neu