Epicardium and Myocardium Separate From a Common Precursor Pool by Crosstalk Between Bone Morphogenetic Protein– and Fibroblast Growth Factor–Signaling Pathways

Using DiI tracing, we show that the epicardium separates from the same precursor pool as the inflow myocardium

Bram van Wijk; Gert van den Berg; Radwan Abu-Issa; Phil Barnett; Saskia van der Velden; Martina Schmidt; Jan M. Ruijter; Margaret L. Kirby; Antoon F.M. Moorman; Maurice J.B. van den Hoff

2009

Scholarcy highlights

  • Using DiI tracing, we show that theepicardium separates from the same precursor pool as the inflow myocardium. We show that this lineage separation is regulated by a crosstalk between bone morphogenetic protein signaling and fibroblast growth factor signaling
  • Embryos exposed to recombinant FGF2 in vivo show enhanced epicardium formation, whereas a misbalance between FGF and BMP by Mek1/2 inhibition and BMP stimulation causes a developmental arrest of the epicardium and enhances myocardium formation at the inflow of the heart
  • Our data show that FGF signaling via Mek1/2 is dominant over BMP signaling via Smad and is required to separate the epicardial lineage from precardiac mesoderm
  • I n contrast to the adult heart, the embryonic heart tube is devoid of nonmyocardial cells and an epicardium, consisting of an outer myocardial and an inner endocardial layer separated by cardiac jelly
  • We show that BMP-mediated myocardial differentiation is inhibited by FGF signaling via Mek1/2 and extracellular signal-regulated kinase1/2, which is required to separate the epicardial lineage from a common progenitor pool
  • These observations suggest that theepicardium and epicardial-derived cells contribute to the cardiac stem cells population observed in several studies. In this respect, the presence of both P-Smad and P-extracellular signal-regulated kinase in stage 33 epicardium indicates that at later stages a balance between fibroblast growth factor and bone morphogenetic protein signaling might be operational

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