Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 110, Issue 33, Pages 13416-13421Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1309810110
Keywords
TRAP; cardiac regeneration; interleukin; inflammation; endocardium
Categories
Funding
- American Heart Association [12FTF11660037]
- National Heart, Lung, and Blood Institute (NHLBI) Medical Scientist Training Program supplement
- National Institutes of Health Training Grant [T32 HL007101-35]
- NHLBI [HL081674]
- Mandel Foundation
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Certain lower vertebrates like zebrafish activate proliferation of spared cardiomyocytes after cardiac injury to regenerate lost heart muscle. Here, we used translating ribosome affinity purification to profile translating RNAs in zebrafish cardiomyocytes during heart regeneration. We identified dynamic induction of several Jak1/Stat3 pathway members following trauma, events accompanied by cytokine production. Transgenic Stat3 inhibition in cardiomyocytes restricted injury-induced proliferation and regeneration, but did not reduce cardiogenesis during animal growth. The secreted protein Rln3a was induced in a Stat3-dependent manner by injury, and exogenous Rln3 delivery during Stat3 inhibition stimulated cardiomyocyte proliferation. Our results identify an injury-specific cardiomyocyte program essential for heart regeneration.
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