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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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Double immunostaining of  normal (+/+) and β1- (−/−) embryoid bodies for β3 integrin and PECAM  (A–D), and αv integrin and PECAM  (E–H). Normal and mutant ES cells  were differentiated for 20 d, fixed and  stained for PECAM (A and C, red) and β3  (B and D, green), or PECAM (E and G,  red) and αv (F and H, green), respectively. In normal embryoid bodies large  vessels stain for PECAM (A and C) and  β3 (B), or αv integrin (D). In β1-  embryoid bodies the vessel diameters  are smaller but the staining for PECAM  (E and G), β3 (D), and αv (H) is similar,  like in normal bodies. Note the high  background for αv staining, which is expressed on many PECAM-negative cells  in the embryoid bodies. Bar, 15 μm.
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Figure 12: Double immunostaining of normal (+/+) and β1- (−/−) embryoid bodies for β3 integrin and PECAM (A–D), and αv integrin and PECAM (E–H). Normal and mutant ES cells were differentiated for 20 d, fixed and stained for PECAM (A and C, red) and β3 (B and D, green), or PECAM (E and G, red) and αv (F and H, green), respectively. In normal embryoid bodies large vessels stain for PECAM (A and C) and β3 (B), or αv integrin (D). In β1- embryoid bodies the vessel diameters are smaller but the staining for PECAM (E and G), β3 (D), and αv (H) is similar, like in normal bodies. Note the high background for αv staining, which is expressed on many PECAM-negative cells in the embryoid bodies. Bar, 15 μm.

Mentions: Proliferating endothelial cells express large amounts of αvβ3 and αvβ5 integrins. To determine whether the expression of β3 or αv integrin is altered on β1- endothelial cells, normal and β1- embryoid bodies were double-immunostained for either PECAM and β3 integrin (Fig. 12, A–D), or PECAM and αv integrin (Fig. 12, E–H), respectively. Vessels in embryoid bodies derived from normal and β1- ES cells express similar amounts of β3 (Fig. 12, B and D) and αv integrin (Fig. 12, F and H). These data indicate that the absence of β1 integrin is not associated with an altered expression of other endothelial cell integrins.


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)

Double immunostaining of  normal (+/+) and β1- (−/−) embryoid bodies for β3 integrin and PECAM  (A–D), and αv integrin and PECAM  (E–H). Normal and mutant ES cells  were differentiated for 20 d, fixed and  stained for PECAM (A and C, red) and β3  (B and D, green), or PECAM (E and G,  red) and αv (F and H, green), respectively. In normal embryoid bodies large  vessels stain for PECAM (A and C) and  β3 (B), or αv integrin (D). In β1-  embryoid bodies the vessel diameters  are smaller but the staining for PECAM  (E and G), β3 (D), and αv (H) is similar,  like in normal bodies. Note the high  background for αv staining, which is expressed on many PECAM-negative cells  in the embryoid bodies. Bar, 15 μm.
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Related In: Results  -  Collection

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Figure 12: Double immunostaining of normal (+/+) and β1- (−/−) embryoid bodies for β3 integrin and PECAM (A–D), and αv integrin and PECAM (E–H). Normal and mutant ES cells were differentiated for 20 d, fixed and stained for PECAM (A and C, red) and β3 (B and D, green), or PECAM (E and G, red) and αv (F and H, green), respectively. In normal embryoid bodies large vessels stain for PECAM (A and C) and β3 (B), or αv integrin (D). In β1- embryoid bodies the vessel diameters are smaller but the staining for PECAM (E and G), β3 (D), and αv (H) is similar, like in normal bodies. Note the high background for αv staining, which is expressed on many PECAM-negative cells in the embryoid bodies. Bar, 15 μm.
Mentions: Proliferating endothelial cells express large amounts of αvβ3 and αvβ5 integrins. To determine whether the expression of β3 or αv integrin is altered on β1- endothelial cells, normal and β1- embryoid bodies were double-immunostained for either PECAM and β3 integrin (Fig. 12, A–D), or PECAM and αv integrin (Fig. 12, E–H), respectively. Vessels in embryoid bodies derived from normal and β1- ES cells express similar amounts of β3 (Fig. 12, B and D) and αv integrin (Fig. 12, F and H). These data indicate that the absence of β1 integrin is not associated with an altered expression of other endothelial cell integrins.

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