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© The Rockefeller University Press, 0021-9525/1997//265 $5.00
The Journal of Cell Biology, Volume 139, Number 1, , 1997 265-278

Article

β1 Integrin Is Essential for Teratoma Growth and Angiogenesis



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

* Institute for Anatomy, University of Cologne, 50931 Cologne, Germany; {ddagger} 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 β1 integrin during teratoma formation, we compared teratomas induced by normal and β1-null ES cells. Injection of normal ES cells gave rise to large teratomas. In contrast, β1-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 β1-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 β1-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, β1-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 β1- deficient endothelial cells were absent in teratomas, β1-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 β1-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 β1-null embryoid bodies.

Abbreviations used in this paper: BrdU, bromodeoxyuridine; ECM, extracellular matrix; ES, embryonic stem; PECAM, platelet/endothelial cell adhesion molecule; VEGF, vascular endothelial growth factor; vWF, von Willebrand Factor.

W. Bloch and E. Forsberg have contributed equally to this work.

Address all correspondence to Reinhard Fässler, Max Planck Institut für Biochemie, am Klopferspitz 18 A, 82 152 Martinsried, Germany. Tel.: (49) 89-8578-2215. FAX: (49) 89-8578-2422. e-mail: faessler{at}biochem.mpg.de


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