Abstract

Background: Vascular patterning depends on coordinated timing of arteriovenous specification of endothelial cells and the concomitant hemodynamic forces supplied by the onset of cardiac function. Using a combination of 3D imaging by OPT and embryo registration techniques, we sought to identify structural differences between three different mouse models of cardiovascular perturbation.

Results: Endoglin mutant mice shared a high degree of similarity to Mlc2a mutant mice, which have been shown to have a primary developmental heart defect causing secondary vessel remodeling failures. Dll4 mutant mice, which have well-characterized arterial blood vessel specification defects, showed distinct differences in vascular patterning when compared to the disruptions seen in Mlc2a-/- and Eng-/- models. While Mlc2a-/- and Eng-/- embryos exhibited significantly larger atria than wild-type, Dll4-/- embryos had significantly smaller hearts than wild-type, but this quantitative volume decrease was not limited to the developing atrium. Dll4-/- embryos also had atretic dorsal aortae and smaller trunks, suggesting that the cardiac abnormalities were secondary to primary arterial blood vessel specification defects.

Conclusions: The similarities in Eng-/- and Mlc2a-/- embryos suggest that Eng-/- mice may suffer from a primary heart developmental defect and secondary defects in vessel patterning, while defects in Dll4-/- embryos are consistent with primary defects in vessel patterning.

Department(s)

Biology

Document Type

Article

DOI

https://doi.org/10.1371/journal.pone.0137175

Rights Information

© 2015 Anderson et al. This is an open access article distributedunder the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproductionin any medium, provided the original author and source are credited.

Publication Date

2015

Recommended Citation

Anderson, Gregory A., Ryan S. Udan, Mary E. Dickinson, and R. Mark Henkelman. "Cardiovascular patterning as determined by hemodynamic forces and blood vessel genetics." PloS one 10, no. 9 (2015).

Journal Title

PLOS ONE

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