May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Deletion of a Single Dll4 Allele Alters Retinal Vascular Development in Mice
Author Affiliations & Notes
  • I.B. Lobov
    Eye Research, Regeneron Pharmaceuticals, Inc., Tarrytown, NY
  • R.A. Renard
    Eye Research, Regeneron Pharmaceuticals, Inc., Tarrytown, NY
  • N. Papadopoulos
    Eye Research, Regeneron Pharmaceuticals, Inc., Tarrytown, NY
  • G. Thurston
    Eye Research, Regeneron Pharmaceuticals, Inc., Tarrytown, NY
  • N.W. Gale
    Eye Research, Regeneron Pharmaceuticals, Inc., Tarrytown, NY
  • G.D. Yancopoulos
    Eye Research, Regeneron Pharmaceuticals, Inc., Tarrytown, NY
  • S.J. Wiegand
    Eye Research, Regeneron Pharmaceuticals, Inc., Tarrytown, NY
  • Footnotes
    Commercial Relationships  I.B. Lobov, Regeneron Pharmaceuticals, Inc., E; R.A. Renard, Regeneron Pharmaceuticals, Inc., E; N. Papadopoulos, Regeneron Pharmaceuticals, Inc., E; G. Thurston, Regeneron Pharmaceuticals, Inc., E; N.W. Gale, Regeneron Pharmaceuticals, Inc., E; G.D. Yancopoulos, Regeneron Pharmaceuticals, Inc., E; S.J. Wiegand, Regeneron Pharmaceuticals, Inc., E.
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 3877. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      I.B. Lobov, R.A. Renard, N. Papadopoulos, G. Thurston, N.W. Gale, G.D. Yancopoulos, S.J. Wiegand; Deletion of a Single Dll4 Allele Alters Retinal Vascular Development in Mice . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3877.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose: : Genetic deletion of Dll4, a Notch ligand prominently expressed in the arterial endothelium, causes severe abnormalities in vascular development and remodeling. Deletion of even a single allele results in almost complete embryonic lethality in the C57BL/6:129 hybrid mixed background and less than 50% of embryonic lethality in ICR background. Therefore, to evaluate the role of Dll4 in retinal vascular development, we analyzed retinas of ICR mice heterozygous for Dll4 deletion / lacZ substitution.

Methods: : VelociGene technology was used to replace the entire Dll4 coding region with the ß–galactosidase reporter gene in C57BL/6:129 hybrid mouse embryonic stem cells [Gale N et al., PNAS 101:15949, 2004]. Chimeric males were bred to ICR females. Mice backcrossed for 3 generations to ICR (87.5% ICR) were used for this study. Dll4lacZ/+ mice and wild type littermates were humanely euthanized between postnatal days 5 and 10. After enucleation, retinas were dissected, flat mounted and stained for ß–gal or X–gal to reveal sites of Dll4 expression and/or with FITC–labeled Griffonia simplicifolia lectin I to visualize the vasculature.

Results: : In the developing superficial retinal vasculature, Dll4 was most prominently expressed in the endothelium of differentiated arteries and in specialized "tip cells" located at the leading edge of the growing vascular net. Dll4 was also widely expressed in capillaries throughout the superficial plexus, as well as in the developing deep retinal bed, particularly at the tips and distal stalks of sprouting vessels. Relative to wild–type controls, the retinas of Dll4lacZ/+ mouse pups exhibited several characteristic vascular abnormalities, including delayed arterial differentiation, delayed outgrowth of the superficial plexus, increased numbers of filopodia and vessel sprouts at the leading edge of the vasculature, and increased capillary density in the newly formed primitive capillary network.

Conclusions: : Dll4 negatively regulates vascular sprouting, and promotes the timely development and differentiation of the retinal vasculature.

Keywords: development • growth factors/growth factor receptors • retina 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×