Rescue of the early vascular defects in Tek/Tie2 null mice reveals an essential survival function.
Disruption of the signaling pathways mediated by the receptor tyrosine kinase Tek/Tie2 has shown that this receptor plays a pivotal role in vascularization of the developing embryo. In this report, we have utilized the tetracycline-responsive binary transgenic system to overcome the early lethal cardiovascular defects associated with the tekDeltasp null allele in order to investigate the role of Tek in later stages of vessel growth. We show for the first time in vivo that synchronized loss of tek expression correlates with rapid endothelial cell apoptosis in hemorrhagic regions of the embryo, demonstrating an ongoing requirement for Tek-mediated signal transduction in vascular maintenance.
Jones
N
N
Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Voskas
D
D
Master
Z
Z
Sarao
R
R
Jones
J
J
Dumont
D J
DJ
D000199:Actins / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D001808:Blood Vessels / Q000196:embryology*; D005314:Embryonic and Fetal Development; D004730:Endothelium, Vascular / Q000166:cytology / Q000196:embryology; D006321:Heart / Q000196:embryology; D006470:Hemorrhage; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D051379:Mice; D008822:Mice, Transgenic; D018919:Neovascularization, Physiologic; D020794:Receptor Protein-Tyrosine Kinases / Q000235:genetics / Q000378:metabolism*; D042787:Receptor, TIE-2; D015398:Signal Transduction; D019076:Transgenes; D014841:von Willebrand Factor / Q000378:metabolism
D000199:Actins; D014841:von Willebrand Factor; D020794:Receptor Protein-Tyrosine Kinases; D042787:Receptor, TIE-2