Local fluid shear stress operates a molecular switch to drive fetal semilunar valve extension.
Duc H PhamCharles R DaiBelle Y LinJonathan T ButcherPublished in: Developmental dynamics : an official publication of the American Association of Anatomists (2021)
Low OSS is transduced by endocardial cells into canonical Wnt signaling programs that regulate BMP signaling and endocardial proliferation. In contrast, high LSS induces Notch signaling in endocardial cells, inhibiting Wnt signaling and thereby restricting growth on the ventricular surface. Our results identify a novel mechanically regulated molecular switch, whereby fluid shear stress drives the growth of valve endothelium, orchestrating the extension of the valve in the direction of blood flow.
Keyphrases
- blood flow
- induced apoptosis
- aortic valve
- mitral valve
- signaling pathway
- cell cycle arrest
- aortic stenosis
- left ventricular
- mesenchymal stem cells
- nitric oxide
- magnetic resonance
- public health
- transcatheter aortic valve replacement
- cell proliferation
- computed tomography
- oxidative stress
- atrial fibrillation
- ejection fraction