PUBLICATION

Mature osteoblasts dedifferentiate in response to traumatic bone injury in the zebrafish fin and skull

Authors
Geurtzen, K., Knopf, F., Wehner, D., Huitema, L.F., Schulte-Merker, S., Weidinger, G.
ID
ZDB-PUB-140514-1
Date
2014
Source
Development (Cambridge, England)   141(11): 2225-34 (Journal)
Registered Authors
Huitema, Leonie, Knopf, Franziska, Schulte-Merker, Stefan, Wehner, Daniel, Weidinger, Gilbert
Keywords
none
MeSH Terms
  • Animal Fins/pathology*
  • Animals
  • Animals, Genetically Modified
  • Bone Regeneration
  • Bone and Bones/injuries*
  • Bone and Bones/pathology*
  • Cell Differentiation*
  • Cell Proliferation
  • Fluorescent Dyes
  • Gene Expression Regulation
  • Green Fluorescent Proteins/chemistry
  • Luminescent Proteins/metabolism
  • Necrosis
  • Osteoblasts/cytology*
  • Osteoblasts/metabolism
  • Osteogenesis/drug effects
  • Skull/pathology*
  • Wound Healing
  • Zebrafish
PubMed
24821985 Full text @ Development
Abstract
Zebrafish have an unlimited capacity to regenerate bone after fin amputation. In this process, mature osteoblasts dedifferentiate to osteogenic precursor cells and thus represent an important source of newly forming bone. By contrast, differentiated osteoblasts do not appear to contribute to repair of bone injuries in mammals; rather, osteoblasts form anew from mesenchymal stem cells. This raises the question whether osteoblast dedifferentiation is specific to appendage regeneration, a special feature of the lepidotrichia bone of the fish fin, or a process found more generally in fish bone. Here, we show that dedifferentiation of mature osteoblasts is not restricted to fin regeneration after amputation, but also occurs during repair of zebrafish fin fractures and skull injuries. In both models, mature osteoblasts surrounding the injury downregulate the expression of differentiation markers, upregulate markers of the pre-osteoblast state and become proliferative. Making use of photoconvertible Kaede protein as well as Cre-driven genetic fate mapping, we show that osteoblasts migrate to the site of injury to replace damaged tissue. Our findings suggest a fundamental role for osteoblast dedifferentiation in reparative bone formation in fish and indicate that adult fish osteoblasts display elevated cellular plasticity compared with mammalian bone-forming cells.
Genes / Markers
Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes