Expression of regulatory genes Px6, Otx2, Six3, and FGF2 during newt retina regeneration

Shared Triggering Mechanisms of Retinal Regeneration in Lower Vertebrates and Retinal Rescue in Higher Ones

“…Thus, in human IRBP (interphotoreceptor retinoid-binding protein) principal for transport of visual cycle proteins is down-regulated after NR detachment associated with diabetes retinopathy (Garcia-Ramirez et al, 2009). When we compared RPE in the intact eye and RPE soon after NR removal in Urodela we found by PCR a considerable decrease of RPE65 transcript abundance (Avdonin et al, 2008). Other results strongly suggest that RPE65 in the RPE-derived cells of early retinal regenerate in Urodela is the only reminder after protein degradation or discharge (Chiba et al, 2006).…”

Potential Endogenous Cell Sources for Retinal Regeneration in Vertebrates and Humans: Progenitor Traits and Specialization

“…A study of gene expression in CMZ cells in caudate amphibians, e.g., the newt Pleurodeles waltl , demonstrated the progenitor status of cells in this zone that are involved, along with RPE (see below), in retinal regeneration. The expression of TFs belonging to the EFTF group (Pax6, Otx2, and Six3, as well as c-myc, Prox1, and Pitx2) was also detected [ 51 , 52 , 53 ]. When we saturated adult newt CMZ cells with BrdU, a proliferation marker, this showed that 15–20% of CMZ cells were in the phase of DNA synthesis within a month after the artificial retinal detachment [ 54 ].…”

“…The main events on the pathway of this transformation are as follows: the exit of cells from the RPE layer, their proliferation with the loss of the initial phenotypic features, the formation of a population of cells with neuroblast features, and then their differentiation with the recovery to a fully functioning retina ( Figure 6 and Figure 7 ). All these stages are described from the aspect of cell biology and variations in the expression of genes of newt eye RPE cells [ 51 , 52 , 53 , 119 , 120 , 121 , 122 , 123 ].…”

Genes relacionados con microftalmia y anoftalmia hereditarias

“…Mediante el bloqueo de la actividad del gen Wnt1, SIX3 es capaz de prevenir la expansión anormal de la parte posterior del cerebro en la zona del cerebro anterior. Durante el desarrollo de la retina, SIX3 ha demostrado tener una función clave en la activación de PAX6 para promover el desarrollo del cristalino 34,35 . Además, SIX3 desempeña un papel estratégico en la activación de SOX2 36 .…”