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Title: Lack of endothelial cell survivin causes embryonic defects in angiogenesis, cardiogenesis, and neural tube closure
Authors: Zwerts, Femke ×
Lupu, Florea
De Vriese, Astrid
Pollefeyt, Saskia
Moons, Lieve
Altura, Rachel A
Jiang, Yuying
Maxwell, Patrick H
Hill, Peter
Oh, Hideyasu
Rieker, Claus
Collen, Desire
Conway, Simon J
Conway, Edward #
Issue Date: Jun-2007
Publisher: W.B. Saunders
Series Title: Blood vol:109 issue:11 pages:4742-4752
Abstract: We explored the physiologic role of endothelial cell apoptosis during development by generating mouse embryos lacking the inhibitor of apoptosis protein (IAP) survivin in endothellum. This was accomplished by intercrossing survivin(lox/lox) mice with mice expressing cre recombinase under the control of the endothelial cell specific tiel promoter (tiel-cre mice). Lack of endothelial cell survivin resulted in embryonic lethality. Mutant embryos had prominent and diffuse hemorrhages from embryonic day 9.5 (E9.5) and died before E13.5. Heart development was strikingly abnormal. Survivin-null endocardial lineage cells could not support normal epithelial-mesenchymal transformation (EMT), resulting in hypoplastic endocardial cushions and in utero heart failure. In addition, 30% of mutant embryos had neural tube closure defects (NTDs) that were not caused by bleeding or growth retardation, but were likely due to alterations in the release of soluble factors from endothelial cells that otherwise support neural stem cell proliferation and neurulation. Thus, regulation of endothelial cell survival, and maintenance of vascular integrity by survivin are crucial for normal embryonic angiogenesis, cardiogenesis, and neurogenesis.
URI: 
ISSN: 0006-4971
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Animal Physiology and Neurobiology Section - miscellaneous
Molecular and Vascular Biology
Vesalius Research Centre (-)
× corresponding author
# (joint) last author

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