A newly investigated possibility to repair the damaged retina is the mobilization and directed migration of endogenous BMSCs. Thereby, systemic mobilization by a single dose of NOX-A12, a stromal cell-derived factor 1 (SDF-1)-neutralizing L-aptamer, showed increased homing of BMSCs into the degenerated retina (see green cells below). That was associated with improved visual function when subretinal injection of SDF-1 was additionally performed (graph in the right panel). The redistribution of the cells to the site of injury combined with their observed beneficial effects support the endogenous therapeutic strategy for retinal repair.
Furthermore, activation and differentiation of Müller cells (MCs), the main vertebrate retinal macroglia cell type, play a pivotal role during retinal regeneration in the zebrafish. For this, a laser-based model of retinal de-/regeneration has been established (right panel below; activated MCs around the laser spot in green). We would like to compare the ensuing processes with the mouse, where no endogenous regeneration takes place.
Bi-directional interactions between MCs and cells of the immune system is widely discussed. We will focus on the influence of microglia on MC functions and possible approaches to modify self-repair mechanisms in the mammalian retina.