FGF-2 regulates neurogenesis and degeneration in the dentate gyrus after traumatic brain injury in mice
J. Clin. Invest. Shinichi Yoshimura, et al. 112:1202 doi:10.1172/JCI16618 [Go to this article.]

Figure 2
Effect of gene transfer of FGF-2 with HSV-1 amplicon vector on proliferation of progenitor cells in SGZ after CCI. One hour after sham operation (a) or CCI (panels b–d), HSV-1/mFGF-2 vector (d) or empty vector (c) was injected stereotactically into the injured hippocampus of C57BL/6 mice (see Methods). Mice underwent intraperitoneal injection of BrdU at 6, 7, and 8 days or 13, 14, and 15 after CCI and were killed on day 9 or day 16 (the latter not shown). BrdU staining was detected immunohistochemically as described in Figure 1. Robust BrdU labeling was noted in the SGZ of the ipsilateral DG after CCI (b) vs. sham operation (a), and after CCI in mice injected with HSV-1/mFGF-2 (d) vs. control vector (c). Tissue section coordinate, bregma –1.9 mm. Scale bar: 100 μm. (e) Quantification of BrdU-positive cells in SGZ in C57BL/6 mice injected with HSV-1/mFGF-2 or HSV-1/empty. HSV-1/mFGF-2 or HSV-1/empty was injected into injured hippocampus 1 hour after CCI. BrdU was injected at 6, 7, and 8 days, or 13, 14, and 15 days after CCI, and animals killed on day 9 or 16, respectively. Sham-operated mice were injected with BrdU on days 6, 7, and 8, and killed on day 9. After CCI, mice injected with HSV-1/mFGF-2 (black bars) had a greater number of BrdU-positive cells in SGZ on day 9 vs. HSV-1/empty (gray bar) or after CCI only (white bars). ^†P < 0.05 compared with sham-control. *P < 0.05 compared with HSV-1/empty (n = 6 per group).