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Biochem Biophys Res Commun. 2011 Nov 25;415(3):490-6. doi: 10.1016/j.bbrc.2011.10.100. Epub 2011 Oct 28.

Functions of the Wnt/β-catenin pathway in an anemia-induced zebrafish model of cardiomyopathy are location dependent.

Author information

1
Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, United States.

Abstract

Recent evidence that the heart is not a terminally-differentiated organ has provided more credence to investigations of pathways involved in inducing cardiomyocyte (CM) hyperplasia as a therapy for heart disease. Here, we leveraged zebrafish as a novel vertebrate model of cardiomyopathy to explore the therapeutic potential based on the Wnt/β-catenin signaling. In the anemia-induced zebrafish model of cardiomyopathy (tr265), we detected differently regulated CM hyperplasia and CM hypertrophy in the compact region and the trabecular region. To assess the effects of the Wnt/β-catenin pathway on these two regions, the anemia line was crossed with heat shock-inducible transgenic fish to upregulate or downregulate the pathway. Upregulation resulted in increased cardiomyocyte hyperplasia in the heart and increased cardiomyocyte hypertrophy in the trabecular region, while downregulation resulted in reduced cardiomyocyte hyperplasia in the heart and reduced cardiomyocyte hypertrophy in the trabecular region. Importantly, upregulation of the pathway resulted in improved fish survival, while downregulation decreased it. In summary, our data suggested that (1) the compact region and the trabecular region respond differently during cardiac remodeling; (2) activation of the Wnt/β-catenin pathway might exert a cardioprotective function via promoting cardiomyocyte hyperplasia.

PMID:
22056559
PMCID:
PMC3225602
DOI:
10.1016/j.bbrc.2011.10.100
[Indexed for MEDLINE]
Free PMC Article

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