Am J Physiol Cell Physiol AJP: Regulatory, Integrative and Comparative Physiology
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Am J Physiol Cell Physiol (September 25, 2002). doi:10.1152/ajpcell.00193.2002
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Articles in PresS, published online ahead of print September 25, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00193.2002
Submitted on April 24, 2002
Accepted on September 19, 2002

Fibroblast growth factor 2 promotes microvessel formation from mouse embryonic aorta

Tetsu Akimoto1 and Marc R Hammerman2*

1 Internal Medicine, Washington University School of Medicine, St. Louis, Missouri, USA
2 Internal Medicine, Washington University School of Medicine, St. Louis, Missouri, USA; Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri, USA

* To whom correspondence should be addressed. E-mail: mhammerm{at}im.wustl.edu.

To delineate the roles that oxygen and FGFs play in the process of angiogenesis from the embryonic aorta, we cultured mouse embryonic aorta explants (thoracic level to lateral vessels supplying the mesonephros and metanephros) in a three-dimensional type I collagen gel matrix. During 8 days of culture under 5% O2, but not room air, the addition of fibroblast growth factor 2 (FGF2) to explants, stimulated the formation of Gs-IB4-positive, CD31-positive, Flk-1-positive microvessels in a concentration-dependent manner. FGF2-stimulated microvessel formation was inhibited by sequestration of FGF2 via addition of soluble FGF receptor (FGFR) chimera protein or anti-FGF2 antibodies. FGFR1 and FGFR2 were present on explants. Levels of FGFR1, but not FGFR2 were increased in embryonic aorta cultured under 5% O2 relative to room air. Our data suggest that low oxygen up-regulates FGFR1 expression in embryonic aorta in vitro and renders it more responsive to FGF2.




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