FAK- and TGF-β1-dependent biomechanical alterations in microvascular endothelial cells exposed to fluid shear stress gradients
Abstract
Endothelial cells (EC) form a dynamic monolayer barrier that regulates vascular permeability and is highly sensitive to mechanical cues, including shear stresses (SS) generated by blood flow. While spatial shear stress gradients (SSG) are linked to vascular pathologies such as atherosclerosis, their direct effects on cellular biomechanics across EC subtypes remain underexplored. Here, using an impinging flow device compatible with videomicroscopy, we demonstrate that exposure of two EC types to SSG causes an immediate and sustained two-fold decrease in migration speed, accompanied by enhanced coordination of collective motion and directional migration against the flow. Concurrently, EC traction and monolayer stresses increase acutely upon flow onset and continue to rise linearly over time. Mechanistically, FAK-mediated mechanotransduction governs flow-opposed migration, whereas the time-dependent increase in traction depends on TGF-β1 signaling and actomyosin contractility. Together, these findings identify SSG as key regulators of EC mechanics, collective dynamics, and signaling, with important implications for vascular disease diagnostics and therapeutics.
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BibTeX
@article{sanchezrendon2026tgfβ1dependent,
title = {{FAK- and TGF-β1-dependent biomechanical alterations in microvascular endothelial cells exposed to fluid shear stress gradients}},
author = {Julio César Sánchez-Rendón and Erva Keskin and Nadine Oder and Annalena Reuss and Eleftheria Michalaki and Gerald G. Fuller and Alexander Dunn and Effie E. Bastounis},
journal = {Communications Biology},
year = {2026},
month = nov,
doi = {10.1038/s42003-026-11283-9},
url = {https://www.nature.com/articles/s42003-026-11283-9},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - FAK- and TGF-β1-dependent biomechanical alterations in microvascular endothelial cells exposed to fluid shear stress gradients
AU - Julio César Sánchez-Rendón
AU - Erva Keskin
AU - Nadine Oder
AU - Annalena Reuss
AU - Eleftheria Michalaki
AU - Gerald G. Fuller
AU - Alexander Dunn
AU - Effie E. Bastounis
PY - 2026
DA - 2026/11/03
JO - Communications Biology
DO - 10.1038/s42003-026-11283-9
UR - https://www.nature.com/articles/s42003-026-11283-9
AB - Endothelial cells (EC) form a dynamic monolayer barrier that regulates vascular permeability and is highly sensitive to mechanical cues, including shear stresses (SS) generated by blood flow. While spatial shear stress gradients (SSG) are linked to vascular pathologies such as atherosclerosis, their direct effects on cellular biomechanics across EC subtypes remain underexplored. Here, using an impinging flow device compatible with videomicroscopy, we demonstrate that exposure of two EC types to SSG causes an immediate and sustained two-fold decrease in migration speed, accompanied by enhanced coordination of collective motion and directional migration against the flow. Concurrently, EC traction and monolayer stresses increase acutely upon flow onset and continue to rise linearly over time. Mechanistically, FAK-mediated mechanotransduction governs flow-opposed migration, whereas the time-dependent increase in traction depends on TGF-β1 signaling and actomyosin contractility. Together, these findings identify SSG as key regulators of EC mechanics, collective dynamics, and signaling, with important implications for vascular disease diagnostics and therapeutics.
SN - 2399-3642
ER -