Müller glia-derived PRSS56 is required to sustain ocular axial growth and prevent refractive error

摘要: A mismatch between optical power and ocular axial length results in refractive errors. Uncorrected errors constitute the most common cause of vision loss second leading blindness worldwide. Although retina is known to play a critical role regulating growth development, precise factors mechanisms involved are poorly defined. We have previously identified for secreted serine protease PRSS56 size determination variants been implicated etiology both hyperopia myopia, highlighting its importance development. Here, we use combination genetic mouse models demonstrate that Prss56 mutations reduced act via function mechanism. Using conditional gene targeting strategy, show derived from Muller glia contributes growth, implicating new retinal cell type determination. Importantly, persistent activity required during distinct developmental stages spanning pre- post-eye opening periods ensure optimal growth. Thus, our data provide evidence existence molecule contributing prenatal postnatal human Finally, inactivation rescues elongation model myopia caused by null mutation Egr1. Overall, findings identify as potential therapeutic target modulating aimed at preventing or slowing down which reaching epidemic proportions.