Hyperactive FOXO1 results in lack of tip stalk identity and deficient microvascular regeneration during kidney injury.

ABSTRACT: Loss of the microvascular (MV) network results in tissue ischemia, loss of tissue function, and is a hallmark of chronic diseases. The incorporation of a functional vascular network with that of the host remains a challenge to utilizing engineered tissues in clinically relevant therapies. We showed that vascular-bed-specific endothelial cells (ECs) exhibit differing angiogenic capacities, with kidney microvascular endothelial cells (MVECs) being the most deficient, and sought to explore the underlying mechanism. Constitutive activation of the phosphatase PTEN in kidney MVECs resulted in impaired PI3K/AKT activity in response to vascular endothelial growth factor (VEGF). Suppression of PTEN in vivo resulted in microvascular regeneration, but was insufficient to improve tissue function. Prom

SUBMITTER: Dang LTH 

PROVIDER: S-EPMC5567800 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature