PUBLICATION

Inflammation Regulates the Multi-Step Process of Retinal Regeneration in Zebrafish

Authors
Nagashima, M., Hitchcock, P.F.
ID
ZDB-PUB-210501-2
Date
2021
Source
Cells   10(4): (Review)
Registered Authors
Hitchcock, Peter
Keywords
Müller glia, cytokine, damage, microglia, photoreceptor, proliferation, reprogramming
MeSH Terms
  • Animals
  • Cellular Reprogramming
  • Ependymoglial Cells/pathology
  • Inflammation/pathology*
  • Neurogenesis
  • Regeneration/physiology*
  • Retina/physiopathology*
  • Zebrafish/physiology*
PubMed
33916186 Full text @ Cells
Abstract
The ability to regenerate tissues varies between species and between tissues within a species. Mammals have a limited ability to regenerate tissues, whereas zebrafish possess the ability to regenerate almost all tissues and organs, including fin, heart, kidney, brain, and retina. In the zebrafish brain, injury and cell death activate complex signaling networks that stimulate radial glia to reprogram into neural stem-like cells that repair the injury. In the retina, a popular model for investigating neuronal regeneration, Müller glia, radial glia unique to the retina, reprogram into stem-like cells and undergo a single asymmetric division to generate multi-potent retinal progenitors. Müller glia-derived progenitors then divide rapidly, numerically matching the magnitude of the cell death, and differentiate into the ablated neurons. Emerging evidence reveals that inflammation plays an essential role in this multi-step process of retinal regeneration. This review summarizes the current knowledge of the inflammatory events during retinal regeneration and highlights the mechanisms whereby inflammatory molecules regulate the quiescence and division of Müller glia, the proliferation of Müller glia-derived progenitors and the survival of regenerated neurons.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping