PUBLICATION

Fgf-dependent glial cell bridges facilitate spinal cord regeneration in zebrafish

Authors
Goldshmit, Y., Sztal, T.E., Jusuf, P.R., Hall, T.E., Nguyen-Chi, M., and Currie, P.D.
ID
ZDB-PUB-120604-1
Date
2012
Source
The Journal of neuroscience : the official journal of the Society for Neuroscience   32(22): 7477-7492 (Journal)
Registered Authors
Currie, Peter D., Goldshmit, Yona, Hall, Thomas, Jusuf, Patricia, Sztal, Tamar Esther
Keywords
none
MeSH Terms
  • Analysis of Variance
  • Animals
  • Animals, Genetically Modified
  • Bromodeoxyuridine/metabolism
  • Cell Differentiation/drug effects
  • Cell Differentiation/genetics
  • Cell Movement/drug effects
  • Cell Movement/genetics
  • Cell Proliferation/drug effects
  • Dextrans
  • Disease Models, Animal
  • Enzyme Inhibitors/pharmacology
  • Fibroblast Growth Factor 2/pharmacology
  • Fibroblast Growth Factor 3/genetics
  • Fibroblast Growth Factor 3/metabolism
  • Fibroblast Growth Factor 8/pharmacology
  • Gene Expression Regulation/drug effects
  • Gene Expression Regulation/genetics
  • Glial Fibrillary Acidic Protein/genetics
  • Green Fluorescent Proteins/genetics
  • Humans
  • Intermediate Filament Proteins/genetics
  • Intermediate Filament Proteins/metabolism
  • Ki-67 Antigen/metabolism
  • Mitogen-Activated Protein Kinase Kinases/genetics
  • Mitogen-Activated Protein Kinase Kinases/metabolism
  • Motor Activity/drug effects
  • Motor Activity/genetics
  • Nerve Regeneration/drug effects
  • Nerve Regeneration/physiology*
  • Nerve Tissue Proteins/genetics
  • Nerve Tissue Proteins/metabolism
  • Nestin
  • Neuroglia/drug effects
  • Neuroglia/physiology*
  • Pyrroles/pharmacology
  • RNA, Messenger
  • Receptor, Fibroblast Growth Factor, Type 1/genetics
  • Recovery of Function
  • Rhodamines
  • Signal Transduction/drug effects
  • Signal Transduction/genetics*
  • Spinal Cord Injuries/pathology*
  • Spinal Cord Injuries/physiopathology*
  • Time Factors
  • Zebrafish
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
22649227 Full text @ J. Neurosci.
Abstract

Adult zebrafish show a remarkable capacity to regenerate their spinal column after injury, an ability that stands in stark contrast to the limited repair that occurs within the mammalian CNS post-injury. The reasons for this interspecies difference in regenerative capacity remain unclear. Here we demonstrate a novel role for Fgf signaling during glial cell morphogenesis in promoting axonal regeneration after spinal cord injury. Zebrafish glia are induced by Fgf signaling, to form an elongated bipolar morphology that forms a bridge between the two sides of the resected spinal cord, over which regenerating axons actively migrate. Loss of Fgf function inhibits formation of this “glial bridge” and prevents axon regeneration. Despite the poor potential for mammalian axonal regeneration, primate astrocytes activated by Fgf signaling adopt a similar morphology to that induced in zebrafish glia. This suggests that differential Fgf regulation, rather than intrinsic cell differences, underlie the distinct responses of mammalian and zebrafish glia to injury.

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Human Disease / Model
Sequence Targeting Reagents
Fish
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