FIG. 2.

Treatment with rAAV2/5.CMV.Epo or rAAV2/5.CMV.EpoR76E protects the optic nerve of DBA/2J mice with exceedingly high IOP (≥25 mmHg) from glaucomatous axonal degeneration. (A) Bright-field micrographs of optic nerve cross-sections (original magnification, 60×) stained with p-phenylenediamine (PPD). Nerves from preglaucomatous mice (3 months old) have a high density of healthy axons (top left, white arrow). At 10 months of age optic nerves from control mice (rAAV2/5.CMV.eGFP) had profound axonal degeneration marked by the loss of healthy axons, increased sick/dying axons (top right, solid arrows), and gliosis (top right, open arrow). The majority of optic nerves from mice that were treated with either Epo vector (bottom left and right) had little or no axonal degeneration. (B) Bar graph of the number of healthy axons per optic nerve. Data represent means±SEM, and statistical analysis was performed by one-way analysis of variance with pair-wise Bonferroni post hoc test; **p≤0.001 versus rAAV2/5.CMV.eGFP. There was no statistically significant difference between the preglaucomatous, rAAV2/5.CMV.Epo, and rAAV2/5.CMV.EpoR76E groups.