High Shear Stress Reduces ERG Causing Endothelial-Mesenchymal Transition and Pulmonary Arterial Hypertension.

ABSTRACT:

Background

Computational modeling indicated that pathological high shear stress (HSS; 100 dyn/cm²) is generated in pulmonary arteries (PAs; 100-500 µm) in congenital heart defects causing PA hypertension (PAH) and in idiopathic PAH with occlusive vascular remodeling. Endothelial-to-mesenchymal transition (EndMT) is a feature of PAH. We hypothesize that HSS induces EndMT, contributing to the initiation and progression of PAH.

Methods

We used the Ibidi perfusion system to determine whether HSS applied to human PA endothelial cells (ECs) induces EndMT when compared with physiological laminar shear stress (15 dyn/cm²). The mechanism was investigated and targeted to prevent PAH in a mouse with HSS induced by an aortocaval shunt.

Results

EndMT, a featu

SUBMITTER: Shinohara T 

PROVIDER: S-EPMC11753934 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature