Abstract
The use of model systems that are capable of robust, spontaneous retina regeneration has allowed for the identification of genetic pathways and components that are required for retina regeneration. Complemented by mouse models in which retina regeneration can be induced after forced expression of key factors, altered chromatin accessibility, or inhibition of kinase/signaling cascades, a clearer picture of the key regulatory events that control retina regeneration is emerging. In all cases, Müller glia (MG) serve as an adult retinal stem cell that must be reprogrammed to allow for regeneration, with the end goal being to understand why regenerative pathways are blocked in mammals, but spontaneous in other vertebrates such as zebrafish. miRNAs have emerged as key gene regulatory molecules that control both development and regeneration in vertebrates. Here, we focus on a small subset of miRNAs that control MG reprogramming during retina regeneration and have the potential to serve as therapeutic targets for treatment of visual disorders and damage.
Highlights
In mammals and humans, the extent of spontaneous repair after retina injury or disease is either non-existent or extremely limited (Karl and Reh, 2010)
MiRNAs regulate gene expression by binding to 3′ UTR elements leading to deadenylation and subsequent degradation of mRNA targets (Giraldez et al, 2006; Guo et al, 2010)
Further work is required to identify the complete set of miRNAs that regulate retina regeneration and the target genes they control
Summary
The extent of spontaneous repair after retina injury or disease is either non-existent or extremely limited (Karl and Reh, 2010). Rather than regenerate, damaged mammalian retinas commonly undergo reactive gliosis and scar formation (Bringmann et al, 2006). This lack of a complete regenerative response to damage directly limits the treatment options for retinal based diseases such as age-related macular degeneration or Stargardt’s disease (Link and Collery, 2015; Zarbin, 2016). Zebrafish have the ability to regenerate a large array of tissues and organs (Gemberling et al, 2013). One goal for these studies is to determine the factors and pathways that allow for persistent and spontaneous regeneration. We will focus on the explicit role of miRNAs during MG reprogramming
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