PUBLICATION

Regeneration of cryoinjury induced necrotic heart lesions in zebrafish is associated with epicardial activation and cardiomyocyte proliferation

Authors
Schnabel, K., Wu, C.C., Kurth, T., and Weidinger, G.
ID
ZDB-PUB-110519-18
Date
2011
Source
PLoS One   6(4): e18503 (Journal)
Registered Authors
Schnabel, Kristin, Weidinger, Gilbert
Keywords
none
MeSH Terms
  • Heart Diseases/physiopathology*
  • Animals
  • Regeneration*
  • Zebrafish
  • Myocardium/pathology*
  • Cold Temperature*
  • Cell Proliferation*
  • Pericardium/pathology*
(all 8)
PubMed
21533269 Full text @ PLoS One
Abstract
In mammals, myocardial cell death due to infarction results in scar formation and little regenerative response. In contrast, zebrafish have a high capacity to regenerate the heart after surgical resection of myocardial tissue. However, whether zebrafish can also regenerate lesions caused by cell death has not been tested. Here, we present a simple method for induction of necrotic lesions in the adult zebrafish heart based on cryoinjury. Despite widespread tissue death and loss of cardiomyocytes caused by these lesions, zebrafish display a robust regenerative response, which results in substantial clearing of the necrotic tissue and little scar formation. The cellular mechanisms underlying regeneration appear to be similar to those activated in response to ventricular resection. In particular, the epicardium activates a developmental gene program, proliferates and covers the lesion. Concomitantly, mature uninjured cardiomyocytes become proliferative and invade the lesion. Our injury model will be a useful tool to study the molecular mechanisms of natural heart regeneration in response to necrotic cell death.
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Allele Construct Type Affected Genomic Region
li1TgTransgenic Insertion
    twu34TgTransgenic Insertion
      y1TgTransgenic Insertion
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        Marker Marker Type Name
        EGFPEFGEGFP
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