Abstract
Retinal degeneration from inherited gene mutation(s) is a common cause of blindness because of structural and functional alterations in photoreceptors. Accordingly, various approaches are being tested to ameliorate or even cure neuroretinal blinding conditions in susceptible patients by employing neuroprotective agents, gene therapeutics, optogenetics, regenerative therapies, and retinal prostheses. The FVB/NJ mouse strain inherently has a common Pde6b rd1 homozygous allele that renders its progeny blind by the time pups reach weaning age. To study the role matrix metalloproteinase-9 (MMP-9) in retinal structure and function, we examined a global MMP-9 knockout (KO) mouse model that has been engineered on the same FVB/NJ background to test the hypothesis whether lack of MMP-9 activity diminishes neuroretinal degenerative changes and thus helps improve the vision. We compared side-by-side various aspects of the ocular physiology in the wild-type (WT) C57BL/6J, FVB/NJ, and MMP-9 KO strains of mice. The results suggest that MMP-9 KO mice display subdued changes in their retinae as reflected by both structural and functional enhancement in the overall ocular neurophysiological parameters. Altogether, the findings appear to have clinical relevance for targeting conditions wherein MMPs and their overactivities are suspected to play dominant pathophysiological roles in advancing neurodegenerative retinal diseases.