PUBLICATION

Regenerative responses after mild heart injuries for cardiomyocyte proliferation in zebrafish

Authors
Itou, J., Akiyama, R., Pehoski, S., Yu, X., Kawakami, H., Kawakami, Y.
ID
ZDB-PUB-140731-6
Date
2014
Source
Developmental dynamics : an official publication of the American Association of Anatomists   243(11): 1477-86 (Journal)
Registered Authors
Akiyama, Ryutaro, Kawakami, Yasuhiko
Keywords
Cardiomyocytes, Endothelial cells, Epicardial cells, Heart, Regeneration, Zebrafish
MeSH Terms
  • Animals
  • Cell Proliferation/physiology*
  • Endothelial Cells/metabolism
  • Heart Injuries/physiopathology*
  • Heart Ventricles/physiopathology*
  • Heart Ventricles/surgery
  • Histological Techniques
  • Image Processing, Computer-Assisted
  • In Situ Hybridization
  • Myocytes, Cardiac/physiology*
  • Regeneration/physiology*
  • Retinal Dehydrogenase/metabolism
  • T-Box Domain Proteins/metabolism
  • WT1 Proteins/metabolism
  • Wound Healing/physiology
  • Zebrafish/physiology*
  • Zebrafish Proteins/metabolism
PubMed
25074230 Full text @ Dev. Dyn.
Abstract
Background: The zebrafish heart regenerates after various severe injuries. Common processes of heart regeneration are cardiomyocyte proliferation, activation of epicardial tissue and neovascularization. In order to further characterize heart regeneration processes, we introduced milder injuries and compared responses to those induced by ventricular apex resection, a widely used injury method. We used scratching of the ventricular surface and puncturing of the ventricle with a fine tungsten needle as injury inducing techniques. Results: Scratching the ventricular surface induced subtle cardiomyocyte proliferation and responses of the epicardium. Endothelial cell accumulation was limited to the surface of the heart. Ventricular puncture induced cardiomyocyte proliferation, endocardial and epicardial activation and neo-vascularization, similar to the resection method. However, the degree of the responses was milder, correlating with milder injury. Sham operation induced epicardial aldh1a2 expression but not tbx18 and WT1. Conclusions: Puncturing the ventricle induces responses equivalent to resection at milder degrees in a shorter time frame and would be used as simple injury model. Scratching the ventricle did not induce heart regeneration and would be used for studying wound responses to epicardium.
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