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J. Cell Biol.
© The Rockefeller University Press
0021-9525/97/10/265/14 $2.00
Volume 139, Number 1, October 6, 1997 265-278

beta 1 Integrin Is Essential for Teratoma Growth and Angiogenesis

Wilhelm Bloch,* Erik Forsberg,Dagger Sylvia Lentini,* Cord Brakebusch,Dagger Karl Martin,Dagger Hans W. Krell,§ Ulrich H. Weidle,§ Klaus Addicks,* and Reinhard FässlerDagger

* Institute for Anatomy, University of Cologne, 50931 Cologne, Germany; Dagger  Max Planck Institute of Biochemistry, 82152 Martinsried, Germany; and § Boehringer Mannheim, 82372 Penzberg, Germany

Teratomas are benign tumors that form after ectopic injection of embryonic stem (ES) cells into mice and contain derivatives of all primitive germ layers. To study the role of beta 1 integrin during teratoma formation, we compared teratomas induced by normal and beta 1-null ES cells. Injection of normal ES cells gave rise to large teratomas. In contrast, beta 1-null ES cells either did not grow or formed small teratomas with an average weight of <5% of that of normal teratomas. Histological analysis of beta 1-null teratomas revealed the presence of various differentiated cells, however, a much lower number of host-derived stromal cells than in normal teratomas. Fibronectin, collagen I, and nidogen were expressed but, in contrast to normal teratomas, diffusely deposited in beta 1-null teratomas. Basement membranes were present but with irregular shape and detached from the cell surface.

Normal teratomas had large blood vessels with a smooth inner surface, containing both host- and ES cell-derived endothelial cells. In contrast, beta 1-null teratomas had small vessels that were loosely embedded into the connective tissue. Furthermore, endothelial cells were always of host-derived origin and formed blood vessels with an irregular inner surface. Although beta 1- deficient endothelial cells were absent in teratomas, beta 1-null ES cells could differentiate in vitro into endothelial cells. The formation of a complex vasculature, however, was significantly delayed and of poor quality in beta 1-null embryoid bodies. Moreover, while vascular endothelial growth factor induced proliferation of endothelial cells as well as an extensive branching of blood vessels in normal embryoid bodies, it had no effect in beta 1-null embryoid bodies.


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