Translational profiling of cardiomyocytes identifies an early Jak1/Stat3 injury response required for zebrafish heart regeneration

被引：175

作者：

Fang, Yi

Gupta, Vikas

Karra, Ravi

Holdway, Jennifer E.

Kikuchi, Kazu

Poss, Kenneth D. ^{[1
]}

机构：

[1] Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2013年 / 110卷 / 33期

基金：

美国国家卫生研究院;

关键词：

TRAP; cardiac regeneration; interleukin; inflammation; endocardium; MYOCARDIAL REGENERATION; CARDIAC FIBROBLASTS; SIGNAL TRANSDUCER; STAT3; PROLIFERATION; ACTIVATION; SURVIVAL; GROWTH; CELLS; INFLAMMATION;

D O I：

10.1073/pnas.1309810110

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];

摘要：

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.

引用

页码：13416 / 13421

页数：6

共 53 条

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