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Arterial pole progenitors interpret opposing FGF/BMP signals to proliferate or differentiate.

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Date
2010-09
Authors
Hutson, MR
Zeng, XL
Kim, AJ
Antoon, E
Harward, S
Kirby, ML
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Abstract
During heart development, a subpopulation of cells in the heart field maintains cardiac potential over several days of development and forms the myocardium and smooth muscle of the arterial pole. Using clonal and explant culture experiments, we show that these cells are a stem cell population that can differentiate into myocardium, smooth muscle and endothelial cells. The multipotent stem cells proliferate or differentiate into different cardiovascular cell fates through activation or inhibition of FGF and BMP signaling pathways. BMP promoted myocardial differentiation but not proliferation. FGF signaling promoted proliferation and induced smooth muscle differentiation, but inhibited myocardial differentiation. Blocking the Ras/Erk intracellular pathway promoted myocardial differentiation, while the PLCgamma and PI3K pathways regulated proliferation. In vivo, inhibition of both pathways resulted in predictable arterial pole defects. These studies suggest that myocardial differentiation of arterial pole progenitors requires BMP signaling combined with downregulation of the FGF/Ras/Erk pathway. The FGF pathway maintains the pool of proliferating stem cells and later promotes smooth muscle differentiation.
Type
Journal article
Subject
Animals
Arteries
Body Patterning
Bone Morphogenetic Protein 2
Cell Differentiation
Cell Lineage
Cell Proliferation
Chick Embryo
Fibroblast Growth Factor 8
Gene Expression Regulation, Developmental
Heart
MAP Kinase Signaling System
Muscle, Smooth
Myocardium
Quail
Stem Cells
Tissue Culture Techniques
Permalink
https://hdl.handle.net/10161/4176
Published Version (Please cite this version)
10.1242/dev.051565
Publication Info
Hutson, MR; Zeng, XL; Kim, AJ; Antoon, E; Harward, S; & Kirby, ML (2010). Arterial pole progenitors interpret opposing FGF/BMP signals to proliferate or differentiate. Development, 137(18). pp. 3001-3011. 10.1242/dev.051565. Retrieved from https://hdl.handle.net/10161/4176.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Hutson

Mary Redmond Hutson

Assistant Professor of Pediatrics
My laboratory is interested in understanding how congenital heart defects occur. In particular I am focused on defects of the conotruncus (or arterial pole) which include persistent truncus arteriosus, double outlet right ventricle, and tetralogy of Fallot. During early stages of heart development the secondary heart field, a population of cardiac stem cells, forms the smooth muscle and myocardial junction of the arterial pole. Another cell population important for arterial pole formation a
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