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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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Weights of teratomas derived from normal (+/+),  β1-heterozygous (+/−), and  β1- (−/−) ES cells. The  mean values were calculated  from 13 +/+, 4 +/−, and 9  −/− teratomas, respectively.  Individual values are designated by an x.
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Figure 2: Weights of teratomas derived from normal (+/+), β1-heterozygous (+/−), and β1- (−/−) ES cells. The mean values were calculated from 13 +/+, 4 +/−, and 9 −/− teratomas, respectively. Individual values are designated by an x.

Mentions: To investigate the growth of β1- tumors in more detail, mice were killed by cervical dislocation and examined under the stereomicroscope. In 9 out of 18 animals injected with β1- ES cells, no tumor could be detected either at the site of injection, or in distant organs. In the remaining nine animals, a small tumor had formed, which was significantly reduced in weight (mean value 47 mg) when compared with tumors derived from normal (0.93 g) or β1 integrin–heterozygous (1.18 g) ES cells (Fig. 2). No difference in tumor growth was observed in mice carrying either a β1- tumor alone or together with a normal or heterozygous tumor.


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)

Weights of teratomas derived from normal (+/+),  β1-heterozygous (+/−), and  β1- (−/−) ES cells. The  mean values were calculated  from 13 +/+, 4 +/−, and 9  −/− teratomas, respectively.  Individual values are designated by an x.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 2: Weights of teratomas derived from normal (+/+), β1-heterozygous (+/−), and β1- (−/−) ES cells. The mean values were calculated from 13 +/+, 4 +/−, and 9 −/− teratomas, respectively. Individual values are designated by an x.
Mentions: To investigate the growth of β1- tumors in more detail, mice were killed by cervical dislocation and examined under the stereomicroscope. In 9 out of 18 animals injected with β1- ES cells, no tumor could be detected either at the site of injection, or in distant organs. In the remaining nine animals, a small tumor had formed, which was significantly reduced in weight (mean value 47 mg) when compared with tumors derived from normal (0.93 g) or β1 integrin–heterozygous (1.18 g) ES cells (Fig. 2). No difference in tumor growth was observed in mice carrying either a β1- tumor alone or together with a normal or heterozygous tumor.

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