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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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Normal (+/+) and β1- (−/−) embryoid bodies immunostained for PECAM. ES cells were differentiated in hanging  drops for 2 d, cultured in bacteriological dishes for another 3 d (which gives a total culture period of 5 d in suspension), and plated on  gelatin-coated cover slips. After various periods on the cover slips (7, 15, 20 d) outgrowth were fixed and stained for PECAM. The culture periods are designated in each picture. Note the presence of blood cells in vessels of normal embryoid body outgrowths (C). Bars:  (A–D) 80 μm; (F) 40 μm.
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Figure 10: Normal (+/+) and β1- (−/−) embryoid bodies immunostained for PECAM. ES cells were differentiated in hanging drops for 2 d, cultured in bacteriological dishes for another 3 d (which gives a total culture period of 5 d in suspension), and plated on gelatin-coated cover slips. After various periods on the cover slips (7, 15, 20 d) outgrowth were fixed and stained for PECAM. The culture periods are designated in each picture. Note the presence of blood cells in vessels of normal embryoid body outgrowths (C). Bars: (A–D) 80 μm; (F) 40 μm.

Mentions: ES cells were cultured for 5 d in suspension to form embryoid bodies, and then were plated on tissue culture dishes. Initially, PECAM-positive cells were aggregated in dense clusters (Fig. 10 A). These clusters then started to form thin tubes and branched. After 7 d on the culture dish about half of the PECAM-positive cells were part of blood vessels in embryoid bodies derived from normal ES cells. After 15 d of incubation, PECAM-positive cell clumps were no longer visible, the blood vessels were significantly grown in diameter, extensively branched (Fig. 10 B), and often contained many blood cells (Fig. 10 C).


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)

Normal (+/+) and β1- (−/−) embryoid bodies immunostained for PECAM. ES cells were differentiated in hanging  drops for 2 d, cultured in bacteriological dishes for another 3 d (which gives a total culture period of 5 d in suspension), and plated on  gelatin-coated cover slips. After various periods on the cover slips (7, 15, 20 d) outgrowth were fixed and stained for PECAM. The culture periods are designated in each picture. Note the presence of blood cells in vessels of normal embryoid body outgrowths (C). Bars:  (A–D) 80 μm; (F) 40 μm.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 10: Normal (+/+) and β1- (−/−) embryoid bodies immunostained for PECAM. ES cells were differentiated in hanging drops for 2 d, cultured in bacteriological dishes for another 3 d (which gives a total culture period of 5 d in suspension), and plated on gelatin-coated cover slips. After various periods on the cover slips (7, 15, 20 d) outgrowth were fixed and stained for PECAM. The culture periods are designated in each picture. Note the presence of blood cells in vessels of normal embryoid body outgrowths (C). Bars: (A–D) 80 μm; (F) 40 μm.
Mentions: ES cells were cultured for 5 d in suspension to form embryoid bodies, and then were plated on tissue culture dishes. Initially, PECAM-positive cells were aggregated in dense clusters (Fig. 10 A). These clusters then started to form thin tubes and branched. After 7 d on the culture dish about half of the PECAM-positive cells were part of blood vessels in embryoid bodies derived from normal ES cells. After 15 d of incubation, PECAM-positive cell clumps were no longer visible, the blood vessels were significantly grown in diameter, extensively branched (Fig. 10 B), and often contained many blood cells (Fig. 10 C).

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