Evidence that FGF receptor signaling is necessary for endoderm-regulated development of precardiac mesoderm. Mech Ageing Dev 1999 Apr 01;108(1):77-85
Date
06/12/1999Pubmed ID
10366041DOI
10.1016/s0047-6374(99)00003-2Scopus ID
2-s2.0-0033119062 (requires institutional sign-in at Scopus site) 17 CitationsAbstract
Endoderm cells in the heart forming region (HFR endoderm) of stage 6 chicken embryos are required to support the proliferation and terminal differentiation of precardiac mesoderm cells in vitro. The endoderm's effect can be substituted by growth factors, including members of the fibroblast growth factor (FGF) family. However, direct implication of FGFs in this process requires evidence that inhibition of FGF signaling interferes with proliferation and/or terminal differentiation. This report examines the consequences of treating endoderm/precardiac mesoderm co-explants with agents that inactivate FGF receptors. Using sodium chlorate, which prevents FGF ligand-receptor interaction, it was observed that the percentage of S-phase precardiac mesoderm cells was markedly reduced, suggesting that cell proliferation was inhibited. To more specifically affect FGF signaling, the explants were treated with an antibody that recognizes an extracellular domain of FGF receptor-1 (FGFR-1). This treatment similarly inhibited cell proliferation. Although both agents modestly delayed cardiac myocyte differentiation as indicated by the contractile function, expression of alpha-sarcomeric actin was not affected. These findings provide additional evidence that an intact FGF signaling pathway is required during heart development.
Author List
Zhu X, Sasse J, Lough JAuthor
John W. Lough PhD Professor in the Cell Biology, Neurobiology and Anatomy department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsChick Embryo
Endoderm
Heart
Receptor Protein-Tyrosine Kinases
Receptor, Fibroblast Growth Factor, Type 1
Receptors, Fibroblast Growth Factor
Signal Transduction
Sodium Chloride