期刊
AUTOPHAGY
卷 8, 期 4, 页码 690-691出版社
LANDES BIOSCIENCE
DOI: 10.4161/auto.19290
关键词
FGF; autophagy; heart development; second heart field; premature differentiation; heart defect
类别
资金
- NCI NIH HHS [R01 CA096824, P50 CA140388, CA140388, R01 CA142862, CA96824, R56 CA096824] Funding Source: Medline
The fibroblast growth factor (FGF) signaling axis plays important roles in heart development. Yet, the molecular mechanism by which the FGF regulates cardiogenesis is not fully understood. Using genetically engineered mouse and in vitro cultured embryoid body (EB) models, we demonstrate that FGF signaling suppresses premature differentiation of heart progenitor cells, as well as autophagy in outflow tract (OFT) myocardiac cells. The FGF also promotes mesoderm differentiation in embryonic stem cells (ESCs) but inhibits cardiomyocyte differentiation of the mesoderm cells at later stages. Furthermore, inhibition of FGF signaling increases myocardial differentiation and autophagy in both ex vivo cultured embryos and EBs, whereas activation of autophagy promotes myocardial differentiation. Thus, a link between FGF signals preventing premature differentiation of heart progenitor cells and suppression of autophagy has been established. These findings provide the first evidence that autophagy plays a role in heart progenitor differentiation, and suggest a new venue to regulate stem/progenitor cell differentiation.
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