Abstract
Our previous work has documented that FGF‐2 is a potent stimulator of both coronary endothelial cell proliferation and tube formation in quail embryos. The current study addressed the role of FGF signaling and Sca‐1+ bone marrow cells (BMC) in coronary tubulogenesis. Embryonic day 6 mouse hearts were explanted onto collagen gels and incubated for 7 days. Tubulogenesis (aggregate tube length), migration distance and cell number were quantified. Exogenous FGF‐2 enhanced tube formation 3‐fold, while adenovirus FGFR‐1DN, which virtually abolishes all FGF signaling, decreased tubulogenesis by about 50%, and markedly inhibited cell proliferation. Soluble adenovirus FGFR‐3 IIIb (or soluble R3IIIb‐Fc), which can bind and inhibit FGF‐1 and FGF‐9, did not significantly inhibit tubulogenesis, but reduced the number of endothelial cells. Addition of sca‐1+ BMC caused only a small (20%) increase in tubulogenesis. The data support the hypothesis that cell proliferation and tube formation are regulated by different FGF ligands.
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