Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 102, Issue 1, Pages 128-133Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0403198102
Keywords
Akt/PKB; angiogenesis; retina
Categories
Funding
- NCI NIH HHS [R01 CA109086, CA 109086] Funding Source: Medline
- NHLBI NIH HHS [R01 HL071049-02, R01 HL071049, 1R01 HL 071049] Funding Source: Medline
Ask authors/readers for more resources
We investigated the functions of Akt during vascular development and remodeling by using an inducible endothelial cell-specific driver of the dominant-active myrAkt. We found that sustained signaling in response to overexpression of myrAkt led to embryonic lethality, edema, and vascular malformations. In addition to the morphological malformations, the vascular phenotype was consistent with a failure in remodeling, such that the normal patterning and vessel hierarchy was disturbed. Examination of the well studied retinal vasculature during the remodeling phases revealed that transient expression of myrAkt was capable of altering the normal response to oxygen-induced remodeling without causing vascular malformations. These findings suggest that physiological levels of Akt signaling modulated microvascular remodeling and support the hypothesis that, although Akt may be required for vascular growth and homeostasis, appropriate downregulation is also an essential aspect of normal vascular patterning.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available