Targeted disruption of the murine VCAM1 gene: essential role of VCAM-1 in chorioallantoic fusion and placentation

Vascular cell adhesion molecule-1 (VCAM-1) is expressed on vascular endothelium in a variety of inflammatory conditions and mediates leukocyte recruitment from blood into tissues. In this study we report a novel role for VCAM-1 in the formation of the umbilical cord and placenta during development....

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Bibliographic Details
Published in:Genes & development 1995-01, Vol.9 (1), p.1-14
Main Authors: Gurtner, G C, Davis, V, Li, H, McCoy, M J, Sharpe, A, Cybulsky, M I
Format: Article
Language:English
Subjects:
Allantois - embryology
Animals
Base Sequence
Cell Adhesion Molecules - genetics
Cell Adhesion Molecules - isolation & purification
Chorion - embryology
Female
Heart Defects, Congenital - embryology
Immunohistochemistry
Integrin alpha4
Integrins - isolation & purification
Leukocyte Count
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Molecular Sequence Data
Placenta - abnormalities
Placenta - embryology
Placentation - genetics
Pregnancy
Tissue Distribution
Umbilical Cord - abnormalities
Umbilical Cord - embryology
Vascular Cell Adhesion Molecule-1
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Summary:Vascular cell adhesion molecule-1 (VCAM-1) is expressed on vascular endothelium in a variety of inflammatory conditions and mediates leukocyte recruitment from blood into tissues. In this study we report a novel role for VCAM-1 in the formation of the umbilical cord and placenta during development. The murine VCAM1 gene was disrupted by targeted homologous recombination, and a distinct phenotype was found in VCAM-1-deficient embryos. At 8.5 days of gestation, the allantois failed to fuse to the chorion, resulting in abnormal placental development and embryonic death within 1-3 days. In addition, a role for VCAM-1 in early placental formation after chorioallantoic fusion was observed. In a minority of VCAM-1-deficient embryos, the allantois was able to fuse with the chorion, but the allantoic mesoderm was abnormally distributed over the chorionic surface. A small number of VCAM-1-deficient embryos survived, presumably by circumventing the placentation defects. They became viable and fertile adult mice with lack of VCAM-1 expression, normal organs, and an elevated number of circulating blood mononuclear leukocytes.
ISSN:0890-9369
1549-5477
DOI:10.1101/gad.9.1.1