ZFIN ID: ZDB-PUB-030102-1
Heart regeneration in zebrafish
Poss, K.D., Wilson, L.G., and Keating, M.T.
Date: 2002
Source: Science (New York, N.Y.)   298(5601): 2188-2190 (Journal)
Registered Authors: Keating, Mark T., Poss, Kenneth D.
Keywords: none
MeSH Terms:
  • Animals
  • Blood Coagulation
  • Bromodeoxyuridine/metabolism
  • Cell Division*
  • Collagen/analysis
  • Fibrin
  • Fibrosis
  • Gene Expression Regulation
  • Heart/physiology*
  • Heart Injuries/pathology
  • Heart Injuries/physiopathology
  • Heart Ventricles/pathology
  • Heart Ventricles/surgery
  • Mitosis
  • Models, Biological
  • Mutation
  • Myocardial Contraction
  • Myocardium/metabolism
  • Myocardium/pathology
  • Myocytes, Cardiac/physiology*
  • Protein-Serine-Threonine Kinases/genetics
  • Protein-Serine-Threonine Kinases/physiology
  • Protein-Tyrosine Kinases/genetics
  • Protein-Tyrosine Kinases/physiology
  • Regeneration*/genetics
  • Regeneration*/physiology
  • Time Factors
  • Ventricular Function
  • Zebrafish/genetics
  • Zebrafish/physiology*
  • Zebrafish Proteins*
PubMed: 12481136 Full text @ Science
ABSTRACT
Cardiac injury in mammals and amphibians typically leads to scarring, with minimal regeneration of heart muscle. Here, we demonstrate histologically that zebrafish fully regenerate hearts within 2 months of 20% ventricular resection. Regeneration occurs through robust proliferation of cardiomyocytes localized at the leading epicardial edge of the new myocardium. The hearts of zebrafish with mutations in the Mps1 mitotic checkpoint kinase, a critical cell cycle regulator, failed to regenerate and formed scars. Thus, injury-induced cardiomyocyte proliferation in zebrafish can overcome scar formation, allowing cardiac muscle regeneration. These findings indicate that zebrafish will be useful for genetically dissecting the molecular mechanisms of cardiac regeneration.
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