Growth factors acting via endothelial cell-specific receptor tyrosine kinases: VEGFs, Angiopoietins, and ephrins in vascular development

Article Abstract:

In vasculogenesis growth factors act via endothelial cell-specific receptor tyrosine kinases. Vascular endothelial growth factors (VEGFs), ephrins and Angiopoietins have roles in vascular development, based on information from studies with knockout mice. The three different growth factor systems act in very different ways. VEGF and Angiopoietins seem to be complementary and coordinated in action. Ephrins seem to be important in later stages, but may be involved in formation of vessel primodia. Complementary expression patterns are important, but overlapping expression of ligands and receptors will likely in time be seen to be mechanistically important. Little is thusfar known about mechanisms of intracellular signaling in endothelial cells and about unique pathways. The available body of knowledge is reviewed.

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Fgf-10 is required for both limb and lung development and exhibits striking functional similarity to Drosophila branchless

Article Abstract:

Fibroblast growth factor (FGF) family members are thought to be involved in various aspects of embroyonic development in vertebrates as well as in adult tissue homeostasis. Fgf-10-deficient mice have been generated. Limb bud initiation was not present in Fgf-10-/- mice, but the fetuses of the mice went on developing until birth, even though they had no limbs, front or back. The mice had no lungs and could not live, but tracheal development was normal. Main-stem bronchial formation and any other pulmonary branching was disrupted. The pulmonary phenotype of the mice is much like that of the Drosophila mutant branchless, which is an Fgf homolog. Fgf-10 is required for apical ectodermal ridge (AER) formation. It acts epistatically upstream of Fgf-8, which is the first known AER marker for mice.

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osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification

Article Abstract:

Osteoprotegerin (OPG) plays a critical role in regulating postnatal bone mass. Experiments with OPG deficient mice also indicates a corelation between medial calcification of the aorta and renal arteries and the protein. This association between osteoporosis and arterial calcification opens possibilities for studying the impact of OPG regulation on these problems.

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