Notch-Tnf signalling is required for development and homeostasis of arterial valves.

ABSTRACT:

Aims

Congenital anomalies of arterial valves are common birth defects, leading to valvar stenosis. With no pharmaceutical treatment that can prevent the disease progression, prosthetic replacement is the only choice of treatment, incurring considerable morbidity and mortality. Animal models presenting localized anomalies and stenosis of congenital arterial valves similar to that of humans are critically needed research tools to uncover developmental molecular mechanisms underlying this devastating human condition.

Methods and results

We generated and characterized mouse models with conditionally altered Notch signalling in endothelial or interstitial cells of developing valves. Mice with inactivation of Notch1 signalling in valvar endothelial cells (VEC) developed congenital

SUBMITTER: Wang Y 

PROVIDER: S-EPMC5837252 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature