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Am J Physiol Regul Integr Comp Physiol (April 11, 2002). doi:10.1152/ajpregu.00699.2001
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Articles in PresS, published online ahead of print April 11, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00699.2001
Submitted on November 26, 2001
Accepted on April 11, 2002

Microvessel formation from mouse embryonic aortic explants is hypoxia and VEGF dependent

Tetsu Akimoto1, Helen Liapis2, and Marc R Hammerman3*

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

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

To delineate the roles that oxygen and VEGF 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 VEGF to explants, stimulated the formation of CD31-positive, Flk-1-positive, Gs-IB4-positive structures in a concentration-dependent manner. Electron microscopy showed the structures to be capillary-like. VEGF-induced capillary-like structure formation was inhibited by sequestration of VEGF via addition of soluble sFlt-1 fusion protein or anti-VEGF antibodies. Expression of Flk-1, but not Flt-1 was increased in embryonic aorta cultured under 5% O2 relative to room air. Our data suggest that low oxygen up-regulates Flk-1 expression in embryonic aorta in vitro and renders it more responsive to VEGF.




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T. Akimoto and M. R. Hammerman
Microvessel formation from mouse aorta is stimulated in vitro by secreted VEGF and extracts from metanephroi
Am J Physiol Cell Physiol, June 1, 2003; 284(6): C1625 - C1632.
[Abstract] [Full Text] [PDF]


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