Premium
Angioblast differentiation is influenced by the local environment: FGF‐2 induces angioblasts and patterns vessel formation in the quail embryo
Author(s) -
Cox Christopher M.,
Poole Thomas J.
Publication year - 2000
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/(sici)1097-0177(200006)218:2<371::aid-dvdy10>3.0.co;2-z
Subject(s) - quail , biology , fibroblast growth factor , somite , fgf and mesoderm formation , microbiology and biotechnology , mesoderm , embryonic stem cell , embryo , vasculogenesis , anatomy , endocrinology , embryogenesis , medicine , ectoderm , stem cell , genetics , receptor , progenitor cell , gene
The embryonic vasculature forms by the segregation, migration, and assembly of angioblasts from mesoderm, a process termed vasculogenesis. The initial role of fibroblast growth factor 2 (FGF‐2) in vascular development appears to be in the induction of endothelial precursors, angioblasts. Quail somites transplanted into chick embryos will give rise to angioblasts of quail origin. The number of angioblasts present within the chimera is dependent on the host environment. Angioblast induction can be demonstrated in vitro by the addition of FGF‐2 to cultures of dissociated somitic mesoderm, as assessed by QH‐1 epitope expression. Manipulation of FGF‐2 concentration in the quail/chick chimeras by FGF‐2 peptide or neutralizing antibody injections increases or decreases angioblast induction in the predicted manner. To better control growth factor release in vivo we have implanted beads that release FGF‐2 into the embryonic environment. FGF‐2 beads implanted into the somite induce angioblast differentiation in the epithelial somite; whereas, beads lateral to the somitic mesoderm induce the formation of ectopic vessels. These studies suggest that FGF‐2 is important for both the induction of angioblasts and the assembly of angioblasts into the initial vasculature pattern. Dev Dyn;218:371–382. © 2000 Wiley‐Liss, Inc.