Mice with targeted mutations in genes required for Notch signal transductio
n die during embryogenesis, displaying overt signs of hemorrhage due to def
ects in their vascular development. Surprisingly, directed expression of a
constitutively active form of Notch4 within mouse endothelial cells produce
s a similar vascular embryonic lethality. Moreover, patients with mutations
in Notch3 exhibit the cerebral vascular disorder, cerebral autosomal domin
ant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL
). These findings underscore the importance of Notch signaling in vascular
development; however, they do not identify the specific functional defect.
Here, we report that Notch1, Notch3, Notch4, Delta4, Jagged1 and Jagged2 ar
e all expressed in arteries, but are not expressed by veins. These findings
identify an aspect of Notch signaling that could contribute to the mechani
sm by which this pathway modulates vascular morphogenesis. (C) 2001 Elsevie
r Science Ireland Ltd. All rights reserved.