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Beta 1 integrin is essential for teratoma growth and angiogenesis.

Bloch W, Forsberg E, Lentini S, Brakebusch C, Martin K, Krell HW, Weidle UH, Addicks K, Fässler R - J. Cell Biol. (1997)

Bottom Line: Furthermore, endothelial cells were always of host-derived origin and formed blood vessels with an irregular inner surface.The formation of a complex vasculature, however, was significantly delayed and of poor quality in beta1- 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- embryoid bodies.

View Article: PubMed Central - PubMed

Affiliation: Institute for Anatomy, University of Cologne, 50931 Cologne, Germany.

ABSTRACT
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 beta1- ES cells. Injection of normal ES cells gave rise to large teratomas. In contrast, beta 1- 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- 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 beta1- 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- 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- ES cells could differentiate in vitro into endothelial cells. The formation of a complex vasculature, however, was significantly delayed and of poor quality in beta1- 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- embryoid bodies.

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Semithin sections of a normal and a β1- teratoma stained with methylene blue and immunostained for vWF. Vessels (V) in  normal teratomas (A) have a smooth inner surface and are tightly embedded within the surrounding tissue (arrows). Vessels of β1-  teratomas (B) have an irregular surface and have lost contacts to the surrounding tissue (arrows). Bar, 20 μm.
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Figure 9: Semithin sections of a normal and a β1- teratoma stained with methylene blue and immunostained for vWF. Vessels (V) in normal teratomas (A) have a smooth inner surface and are tightly embedded within the surrounding tissue (arrows). Vessels of β1- teratomas (B) have an irregular surface and have lost contacts to the surrounding tissue (arrows). Bar, 20 μm.

Mentions: During the analysis of tissue sections derived from β1- teratomas it became evident that also the host cell–derived vasculature has abnormalities. Whereas blood vessels in normal teratomas have a smooth inner surface and are tightly anchored to the surrounding connective tissue (Fig. 9 A), blood vessels in β1- tumors have an irregular inner surface and display large gaps between endothelial cells and the surrounding tissue (Fig. 9 B).


Beta 1 integrin is essential for teratoma growth and angiogenesis.

Bloch W, Forsberg E, Lentini S, Brakebusch C, Martin K, Krell HW, Weidle UH, Addicks K, Fässler R - J. Cell Biol. (1997)

Semithin sections of a normal and a β1- teratoma stained with methylene blue and immunostained for vWF. Vessels (V) in  normal teratomas (A) have a smooth inner surface and are tightly embedded within the surrounding tissue (arrows). Vessels of β1-  teratomas (B) have an irregular surface and have lost contacts to the surrounding tissue (arrows). Bar, 20 μm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2139829&req=5

Figure 9: Semithin sections of a normal and a β1- teratoma stained with methylene blue and immunostained for vWF. Vessels (V) in normal teratomas (A) have a smooth inner surface and are tightly embedded within the surrounding tissue (arrows). Vessels of β1- teratomas (B) have an irregular surface and have lost contacts to the surrounding tissue (arrows). Bar, 20 μm.
Mentions: During the analysis of tissue sections derived from β1- teratomas it became evident that also the host cell–derived vasculature has abnormalities. Whereas blood vessels in normal teratomas have a smooth inner surface and are tightly anchored to the surrounding connective tissue (Fig. 9 A), blood vessels in β1- tumors have an irregular inner surface and display large gaps between endothelial cells and the surrounding tissue (Fig. 9 B).

Bottom Line: Furthermore, endothelial cells were always of host-derived origin and formed blood vessels with an irregular inner surface.The formation of a complex vasculature, however, was significantly delayed and of poor quality in beta1- 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- embryoid bodies.

View Article: PubMed Central - PubMed

Affiliation: Institute for Anatomy, University of Cologne, 50931 Cologne, Germany.

ABSTRACT
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 beta1- ES cells. Injection of normal ES cells gave rise to large teratomas. In contrast, beta 1- 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- 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 beta1- 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- 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- ES cells could differentiate in vitro into endothelial cells. The formation of a complex vasculature, however, was significantly delayed and of poor quality in beta1- 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- embryoid bodies.

Show MeSH
Related in: MedlinePlus