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The conditional inactivation of the beta-catenin gene in endothelial cells causes a defective vascular pattern and increased vascular fragility.

Cattelino A, Liebner S, Gallini R, Zanetti A, Balconi G, Corsi A, Bianco P, Wolburg H, Moore R, Oreda B, Kemler R, Dejana E - J. Cell Biol. (2003)

Bottom Line: We found that early phases of vasculogenesis and angiogenesis were not affected in mutant embryos; however, vascular patterning in the head, vitelline, umbilical vessels, and the placenta was altered.These changes paralleled a decrease in cell-cell adhesion strength and an increase in paracellular permeability.We conclude that in vivo, the absence of beta-catenin significantly reduces the capacity of endothelial cells to maintain intercellular contacts.

View Article: PubMed Central - PubMed

Affiliation: FIRC Institute of Molecular Oncology, 16-20139, Milan, Italy.

ABSTRACT
Using the Cre/loxP system we conditionally inactivated beta-catenin in endothelial cells. We found that early phases of vasculogenesis and angiogenesis were not affected in mutant embryos; however, vascular patterning in the head, vitelline, umbilical vessels, and the placenta was altered. In addition, in many regions, the vascular lumen was irregular with the formation of lacunae at bifurcations, vessels were frequently hemorrhagic, and fluid extravasation in the pericardial cavity was observed. Cultured beta-catenin -/- endothelial cells showed a different organization of intercellular junctions with a decrease in alpha-catenin in favor of desmoplakin and marked changes in actin cytoskeleton. These changes paralleled a decrease in cell-cell adhesion strength and an increase in paracellular permeability. We conclude that in vivo, the absence of beta-catenin significantly reduces the capacity of endothelial cells to maintain intercellular contacts. This may become more marked when the vessels are exposed to high or turbulent flow, such as at bifurcations or in the beating heart, leading to fluid leakage or hemorrhages.

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Hemorrhages and fluid extravasation in β-catenin mutant embryos. E10.5 control (A and D) and mutant embryos (B, C, and E). Arrowheads in B and C indicate regions of extended hemorrhages. In the mutants, we observed fluid accumulation in the pericardial cavity (arrow in E in comparison to controls in D) suggesting increase of permeability of cardiac microvasculature.
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fig4: Hemorrhages and fluid extravasation in β-catenin mutant embryos. E10.5 control (A and D) and mutant embryos (B, C, and E). Arrowheads in B and C indicate regions of extended hemorrhages. In the mutants, we observed fluid accumulation in the pericardial cavity (arrow in E in comparison to controls in D) suggesting increase of permeability of cardiac microvasculature.

Mentions: About 50% of the embryos presented hemorrhages in different vascular areas such as the head and the dorsal vessels (Fig. 4, B and C, arrowheads). The heart of the mutant embryos was significantly smaller as compared with the wild type, and frequently showed extensive liquid accumulation in the pericardial cavity (Fig. 4, D and E, arrows).


The conditional inactivation of the beta-catenin gene in endothelial cells causes a defective vascular pattern and increased vascular fragility.

Cattelino A, Liebner S, Gallini R, Zanetti A, Balconi G, Corsi A, Bianco P, Wolburg H, Moore R, Oreda B, Kemler R, Dejana E - J. Cell Biol. (2003)

Hemorrhages and fluid extravasation in β-catenin mutant embryos. E10.5 control (A and D) and mutant embryos (B, C, and E). Arrowheads in B and C indicate regions of extended hemorrhages. In the mutants, we observed fluid accumulation in the pericardial cavity (arrow in E in comparison to controls in D) suggesting increase of permeability of cardiac microvasculature.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2172846&req=5

fig4: Hemorrhages and fluid extravasation in β-catenin mutant embryos. E10.5 control (A and D) and mutant embryos (B, C, and E). Arrowheads in B and C indicate regions of extended hemorrhages. In the mutants, we observed fluid accumulation in the pericardial cavity (arrow in E in comparison to controls in D) suggesting increase of permeability of cardiac microvasculature.
Mentions: About 50% of the embryos presented hemorrhages in different vascular areas such as the head and the dorsal vessels (Fig. 4, B and C, arrowheads). The heart of the mutant embryos was significantly smaller as compared with the wild type, and frequently showed extensive liquid accumulation in the pericardial cavity (Fig. 4, D and E, arrows).

Bottom Line: We found that early phases of vasculogenesis and angiogenesis were not affected in mutant embryos; however, vascular patterning in the head, vitelline, umbilical vessels, and the placenta was altered.These changes paralleled a decrease in cell-cell adhesion strength and an increase in paracellular permeability.We conclude that in vivo, the absence of beta-catenin significantly reduces the capacity of endothelial cells to maintain intercellular contacts.

View Article: PubMed Central - PubMed

Affiliation: FIRC Institute of Molecular Oncology, 16-20139, Milan, Italy.

ABSTRACT
Using the Cre/loxP system we conditionally inactivated beta-catenin in endothelial cells. We found that early phases of vasculogenesis and angiogenesis were not affected in mutant embryos; however, vascular patterning in the head, vitelline, umbilical vessels, and the placenta was altered. In addition, in many regions, the vascular lumen was irregular with the formation of lacunae at bifurcations, vessels were frequently hemorrhagic, and fluid extravasation in the pericardial cavity was observed. Cultured beta-catenin -/- endothelial cells showed a different organization of intercellular junctions with a decrease in alpha-catenin in favor of desmoplakin and marked changes in actin cytoskeleton. These changes paralleled a decrease in cell-cell adhesion strength and an increase in paracellular permeability. We conclude that in vivo, the absence of beta-catenin significantly reduces the capacity of endothelial cells to maintain intercellular contacts. This may become more marked when the vessels are exposed to high or turbulent flow, such as at bifurcations or in the beating heart, leading to fluid leakage or hemorrhages.

Show MeSH
Related in: MedlinePlus