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
-
- Spinal Cord Injuries/pathology*
- Spinal Cord Injuries/physiopathology*
- Pyrroles/pharmacology
- Disease Models, Animal
- Signal Transduction/drug effects
- Signal Transduction/genetics*
- Nestin
- Humans
- Zebrafish
- Fibroblast Growth Factor 3/genetics
- Fibroblast Growth Factor 3/metabolism
- Animals
- Neuroglia/drug effects
- Neuroglia/physiology*
- Animals, Genetically Modified
- Green Fluorescent Proteins/genetics
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- Glial Fibrillary Acidic Protein/genetics
- Intermediate Filament Proteins/genetics
- Intermediate Filament Proteins/metabolism
- Ki-67 Antigen/metabolism
- Dextrans
- Gene Expression Regulation/drug effects
- Gene Expression Regulation/genetics
- Fibroblast Growth Factor 8/pharmacology
- Nerve Regeneration/drug effects
- Nerve Regeneration/physiology*
- Mitogen-Activated Protein Kinase Kinases/genetics
- Mitogen-Activated Protein Kinase Kinases/metabolism
- Rhodamines
- Time Factors
- Cell Differentiation/drug effects
- Cell Differentiation/genetics
- Motor Activity/drug effects
- Motor Activity/genetics
- RNA, Messenger
- Fibroblast Growth Factor 2/pharmacology
- Nerve Tissue Proteins/genetics
- Nerve Tissue Proteins/metabolism
- Cell Movement/drug effects
- Cell Movement/genetics
- Enzyme Inhibitors/pharmacology
- Recovery of Function
- Cell Proliferation/drug effects
- Analysis of Variance
- Receptor, Fibroblast Growth Factor, Type 1/genetics
- Bromodeoxyuridine/metabolism
- PubMed
- 22649227 Full text @ J. Neurosci.
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.