Skip to main content
. Author manuscript; available in PMC: 2014 Jul 1.
Published in final edited form as: Exp Eye Res. 2013 May 3;112:106–117. doi: 10.1016/j.exer.2013.04.021

Figure 4. The Jun target, Atf3, suppresses RGC death following CONC.

Figure 4

(A) The expression of Atf3 significantly increased after CONC in Jun+/+ retinas at 2 and 5 days (shown as normalized fold change; *, intra-genotype comparison, P < 0.05). Atf3 expression was not significantly increased after CONC in Jun−/− retinas at 2 and 5 days. In fact, comparing the change in gene expression of Atf3 between Jun+/+ and Jun−/− mice showed that Atf3 expression was significantly attenuated in Jun−/− at both time points after CONC (#, inter-genotype comparison, P < 0.05). Also, Atf3 expression was significantly increased in Jun−/− retinas compared to Jun+/+ retinas prior to injury. (B) Representative images of cleaved caspase-3 (cCASP3) labeled, dying RGCs in Atf3+/+ and Atf3−/− retinal whole mounts. (C) The number of cCASP3 labeled cells was significantly reduced in Atf3−/− retinas at both 3 days and 5 days after CONC (*, P < 0.05 for both time points; N≥5 for both genotypes and time points). (D) Representative images of anti-βIII tubulin (TUJ1) positive RGCs in retinal whole mounts from sham injured and CONC injured eyes 14 days following the insult. (E) Despite the small decrease in cell death in Atf3 deficient mice, Atf3 deficiency did not increase the number of surviving RGCs 14 days after CONC (P = 0.82, N= 6 for genotypes). Scalebar, 25 μm.