Dataset Information

Adult sox10+ Cardiomyocytes Contribute to Myocardial Regeneration in the Zebrafish.

ABSTRACT: During heart regeneration in the zebrafish, fibrotic tissue is replaced by newly formed cardiomyocytes derived from preexisting ones. It is unclear whether the heart is composed of several cardiomyocyte populations bearing different capacity to replace lost myocardium. Here, using sox10 genetic fate mapping, we identify a subset of preexistent cardiomyocytes in the adult zebrafish heart with a distinct gene expression profile that expanded after cryoinjury. Genetic ablation of sox10+ cardiomyocytes impairs cardiac regeneration, revealing that these cells play a role in heart regeneration.

SUBMITTER: Sande-Melon M

PROVIDER: S-EPMC6856760 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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Publications

Adult sox10<sup>+</sup> Cardiomyocytes Contribute to Myocardial Regeneration in the Zebrafish.

Sande-Melón Marcos M Marques Inês J IJ Galardi-Castilla María M Langa Xavier X Pérez-López María M Botos Marius-Alexandru MA Sánchez-Iranzo Héctor H Guzmán-Martínez Gabriela G Ferreira Francisco David Miguel DM Pavlinic Dinko D Benes Vladimir V Bruggmann Rémy R Mercader Nadia N

Cell reports 20191001 4

During heart regeneration in the zebrafish, fibrotic tissue is replaced by newly formed cardiomyocytes derived from preexisting ones. It is unclear whether the heart is composed of several cardiomyocyte populations bearing different capacity to replace lost myocardium. Here, using sox10 genetic fate mapping, we identify a subset of preexistent cardiomyocytes in the adult zebrafish heart with a distinct gene expression profile that expanded after cryoinjury. Genetic ablation of sox10<sup>+</sup> ...[more]

PMID: 31644901

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Project description:Recent studies indicate that mammals, including humans, maintain some capacity to renew cardiomyocytes throughout postnatal life. Yet, there is little or no significant cardiac muscle regeneration after an injury such as acute myocardial infarction. By contrast, zebrafish efficiently regenerate lost cardiac muscle, providing a model for understanding how natural heart regeneration may be blocked or enhanced. In the absence of lineage-tracing technology applicable to adult zebrafish, the cellular origins of newly regenerated cardiac muscle have remained unclear. Using new genetic fate-mapping approaches, here we identify a population of cardiomyocytes that become activated after resection of the ventricular apex and contribute prominently to cardiac muscle regeneration. Through the use of a transgenic reporter strain, we found that cardiomyocytes throughout the subepicardial ventricular layer trigger expression of the embryonic cardiogenesis gene gata4 within a week of trauma, before expression localizes to proliferating cardiomyocytes surrounding and within the injury site. Cre-recombinase-based lineage-tracing of cells expressing gata4 before evident regeneration, or of cells expressing the contractile gene cmlc2 before injury, each labelled most cardiac muscle in the ensuing regenerate. By optical voltage mapping of surface myocardium in whole ventricles, we found that electrical conduction is re-established between existing and regenerated cardiomyocytes between 2 and 4 weeks post-injury. After injury and prolonged fibroblast growth factor receptor inhibition to arrest cardiac regeneration and enable scar formation, experimental release of the signalling block led to gata4 expression and morphological improvement of the injured ventricular wall without loss of scar tissue. Our results indicate that electrically coupled cardiac muscle regenerates after resection injury, primarily through activation and expansion of cardiomyocyte populations. These findings have implications for promoting regeneration of the injured human heart.

Dataset Information

Adult sox10+ Cardiomyocytes Contribute to Myocardial Regeneration in the Zebrafish.

Publications

Adult sox10<sup>+</sup> Cardiomyocytes Contribute to Myocardial Regeneration in the Zebrafish.

Similar Datasets

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