Skip to main content
. 2018 Dec 18;9:633. doi: 10.3389/fgene.2018.00633

FIGURE 4.

FIGURE 4

Downregulation of Sox11 facilitates RGC survival following ONC. (A) Sox11 is partially knocked out by intravitreal injection of AAV2-CMV-Cre-GFP in 4 to 6-week-old Sox11f/f mice. The control group receives AAV2-CMV-GFP. Optic nerve crush is performed 2 weeks after viral vector injection. Twelve days after ONC, Alexa Fluor 647-conjugated cholera toxin B (CTB) is used to label regenerating axons. Two days later mice are sacrificed. (B) For the retinal whole mounts, RGCs are labeled with the pan-RGC marker RBPMS. The number of AAV2-GFP vector transduced RGCs without crush injury is 1782 ± 117.5/mm2. (C) Downregulation of Sox11 in RGCs greatly increases the survival of AAV2 vector transduced RGCs (double labeled by GFP and RBPMS) after ONC as compared to AAV2-CMV-GFP injection with ONC group (357 ± 7.1/mm2 vs. 158 ± 15.7/mm2, n = 4, p = 0.029, Mann–Whitney U-test). (D) The number of total RGCs labeled by RBPMS without crush injury is 3389 ± 92.1/mm2. When comparing the total RGCs labeled by RBPMS, it shows that Sox11 partial knockout in the Sox11f/f mice significantly increases RPBMS-positive RGC survival after ONC as compared to AAV2-CMV-GFP ONC group (1398 ± 63/mm2 vs. 828 ± 23/mm2, n = 4, p = 0.028, Mann–Whitney U-test). Scale bar = 100 μm.