Translational profiling of cardiomyocytes identifies an early Jak1/Stat3 injury response required for zebrafish heart regeneration
- Authors
- Fang, Y., Gupta, V., Karra, R., Holdway, J.E., Kikuchi, K., and Poss, K.D.
- ID
- ZDB-PUB-130816-32
- Date
- 2013
- Source
- Proceedings of the National Academy of Sciences of the United States of America 110(33): 13416-13421 (Journal)
- Registered Authors
- Fang, Yi, Gupta, Vikas, Holdway, Jennifer, Karra, Ravi, Kikuchi, Kazu, Poss, Kenneth D.
- Keywords
- TRAP, cardiac regeneration, interleukin, inflammation, encocardium
- Datasets
- GEO:GSE48914
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Cell Proliferation
- DNA Primers/genetics
- Gene Expression Profiling
- Heart/physiology*
- Histological Techniques
- Immunoprecipitation
- Janus Kinase 1/metabolism*
- Microarray Analysis
- Myocytes, Cardiac/metabolism*
- RNA/isolation & purification
- Regeneration/genetics*
- Relaxin/metabolism
- STAT3 Transcription Factor/metabolism*
- Signal Transduction/physiology*
- Zebrafish/physiology*
- Zebrafish Proteins/metabolism*
- PubMed
- 23901114 Full text @ Proc. Natl. Acad. Sci. USA
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.