Flow-dependent mass transfer may trigger endothelial signaling cascades

Area of Science:

• Biomedical Engineering
• Cell Biology
• Fluid Dynamics

Background:

• Fluid mechanical forces are known to influence endothelial cell signaling.
• The precise mechanisms initiating these signaling pathways, particularly the roles of mechanotransduction versus mass transport, remain unclear.
• Current understanding often relies on criteria correlating signaling with shear stress and shear rate.

Purpose of the Study:

• To investigate the role of mass transfer in endothelial signaling pathways.
• To challenge the prevailing assumption that mechanotransduction is the sole dominant mechanism.
• To evaluate the sufficiency of shear stress and shear rate criteria in determining dominant signaling mechanisms.

Main Methods:

• Computational and experimental analysis of mass-transfer limited systems.
• Systems were subjected to conditions typically used to identify mechanotransduction.
• Investigation focused on isolating the effects of mass transfer independent of direct mechanical force input.

Main Results:

• Mass-transfer limited systems, independent of mechanotransduction, exhibited trends similar to those attributed to mechanotransduction-dominant systems.
• The results indicate that commonly used criteria based on shear stress and shear rate are insufficient to distinguish between mechanotransduction and mass transfer effects.
• The negative control experiments demonstrated that mass transfer alone can mimic established mechanotransduction indicators.

Conclusions:

• The widely accepted criteria correlating shear stress and shear rate are insufficient for determining mechanotransduction-dominant endothelial signaling.
• Mass transfer plays a critical, often underestimated, role in initiating and modulating endothelial signaling cascades.
• Future research must incorporate the significance of mass transfer when investigating hemodynamic force-modulated endothelial responses.