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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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Electronmicroscopy  of normal (A and D) and β1- teratomas and embryoid  bodies (B, C, E, and F). Normal cells in teratomas (A)  and embryoid bodies (D) are  covered by a smooth basement membrane that is strictly  located in close vicinity of  the cell surface (arrowhead).  In β1- teratomas as well  as β1- embryoid bodies,  the basement membranes are  partially detached (B and F,  arrows), multilayered (C), or  show an increased thickness  and a loss of typical structure  (E). Bar, 250 nm.
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Figure 6: Electronmicroscopy of normal (A and D) and β1- teratomas and embryoid bodies (B, C, E, and F). Normal cells in teratomas (A) and embryoid bodies (D) are covered by a smooth basement membrane that is strictly located in close vicinity of the cell surface (arrowhead). In β1- teratomas as well as β1- embryoid bodies, the basement membranes are partially detached (B and F, arrows), multilayered (C), or show an increased thickness and a loss of typical structure (E). Bar, 250 nm.

Mentions: To evaluate whether the ultrastructural morphology of basement membranes is altered by the lack of β1 integrin expression, electronmicroscopy was performed with tumor tissues and embryoid bodies derived from normal and β1- ES cells. In normal tumors and normal embryoid bodies the basement membrane was continuously present along the basal surface of epithelial cells (Fig. 6, A and D) or around muscle cells (not shown) with a constant width that never exceeded 30 nm. In contrast, most cells in β1- teratomas and embryoid bodies were covered by partially detached basement membranes, which resulted in the formation of irregular clefts between plasma membrane and lamina densa (Fig. 6, B and F). In other areas, cells were covered by several layers of basement membranes (Fig. 6 C) or by only partially developed basement membranes (Fig. 6, E and F).


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)

Electronmicroscopy  of normal (A and D) and β1- teratomas and embryoid  bodies (B, C, E, and F). Normal cells in teratomas (A)  and embryoid bodies (D) are  covered by a smooth basement membrane that is strictly  located in close vicinity of  the cell surface (arrowhead).  In β1- teratomas as well  as β1- embryoid bodies,  the basement membranes are  partially detached (B and F,  arrows), multilayered (C), or  show an increased thickness  and a loss of typical structure  (E). Bar, 250 nm.
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Related In: Results  -  Collection

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

Figure 6: Electronmicroscopy of normal (A and D) and β1- teratomas and embryoid bodies (B, C, E, and F). Normal cells in teratomas (A) and embryoid bodies (D) are covered by a smooth basement membrane that is strictly located in close vicinity of the cell surface (arrowhead). In β1- teratomas as well as β1- embryoid bodies, the basement membranes are partially detached (B and F, arrows), multilayered (C), or show an increased thickness and a loss of typical structure (E). Bar, 250 nm.
Mentions: To evaluate whether the ultrastructural morphology of basement membranes is altered by the lack of β1 integrin expression, electronmicroscopy was performed with tumor tissues and embryoid bodies derived from normal and β1- ES cells. In normal tumors and normal embryoid bodies the basement membrane was continuously present along the basal surface of epithelial cells (Fig. 6, A and D) or around muscle cells (not shown) with a constant width that never exceeded 30 nm. In contrast, most cells in β1- teratomas and embryoid bodies were covered by partially detached basement membranes, which resulted in the formation of irregular clefts between plasma membrane and lamina densa (Fig. 6, B and F). In other areas, cells were covered by several layers of basement membranes (Fig. 6 C) or by only partially developed basement membranes (Fig. 6, E and F).

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