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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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Diameter of vessel lumen in normal (+/+) and β1-  (−/−) embryoid bodies. •, −/− PECAM1; □, +/+ PECAM1.  Morphometrical analysis of PECAM-positive vessels after 5 + 20 d  in culture. Normal embryoid bodies have variously sized vessels  with diam up to 70 μm. In β1- embryoid bodies most vessels  have a diam of 10 μm and only a few are larger.
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Figure 11: Diameter of vessel lumen in normal (+/+) and β1- (−/−) embryoid bodies. •, −/− PECAM1; □, +/+ PECAM1. Morphometrical analysis of PECAM-positive vessels after 5 + 20 d in culture. Normal embryoid bodies have variously sized vessels with diam up to 70 μm. In β1- embryoid bodies most vessels have a diam of 10 μm and only a few are larger.

Mentions: When β1- embryoid bodies were analyzed 7 or 15 d after plating, only PECAM-positive cell clusters were found without any signs of vessel formation (Fig. 10 D). After 20 d in culture, a fine network of small vessels began to form in some areas of the embryoid bodies (Fig. 10 E). These vessels were small in diameter and never contained blood cells. In other areas, PECAM-positive cells were still organized in small cell patches, often with loose cell– cell contacts (Fig. 10 F). The mean value of the diameter of normal and β1- vessels in seven embryoid bodies after a 3-wk culture period was 18.1 ± 3.0 μm and 6.8 ± 2.1 μm, respectively (Fig. 11).


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)

Diameter of vessel lumen in normal (+/+) and β1-  (−/−) embryoid bodies. •, −/− PECAM1; □, +/+ PECAM1.  Morphometrical analysis of PECAM-positive vessels after 5 + 20 d  in culture. Normal embryoid bodies have variously sized vessels  with diam up to 70 μm. In β1- embryoid bodies most vessels  have a diam of 10 μm and only a few are larger.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 11: Diameter of vessel lumen in normal (+/+) and β1- (−/−) embryoid bodies. •, −/− PECAM1; □, +/+ PECAM1. Morphometrical analysis of PECAM-positive vessels after 5 + 20 d in culture. Normal embryoid bodies have variously sized vessels with diam up to 70 μm. In β1- embryoid bodies most vessels have a diam of 10 μm and only a few are larger.
Mentions: When β1- embryoid bodies were analyzed 7 or 15 d after plating, only PECAM-positive cell clusters were found without any signs of vessel formation (Fig. 10 D). After 20 d in culture, a fine network of small vessels began to form in some areas of the embryoid bodies (Fig. 10 E). These vessels were small in diameter and never contained blood cells. In other areas, PECAM-positive cells were still organized in small cell patches, often with loose cell– cell contacts (Fig. 10 F). The mean value of the diameter of normal and β1- vessels in seven embryoid bodies after a 3-wk culture period was 18.1 ± 3.0 μm and 6.8 ± 2.1 μm, respectively (Fig. 11).

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