A biomechanical model for fluidization of cells under dynamic strain

Area of Science:

• Biophysics
• Cellular mechanics
• Biotechnology

Background:

• Smooth muscle cells (SMC) are crucial for physiological functions.
• SMC response to mechanical stimuli is complex and not fully understood.
• Stress fibers, composed of actin and myosin, are key mechanical elements in cells.

Purpose of the Study:

• To investigate the asymmetric response of smooth muscle cells to transient stretch-compress (SC) and compress-stretch (CS) maneuvers.
• To elucidate the underlying biomechanical mechanisms driving stress fiber behavior during these maneuvers.
• To identify the role of myosin motor dynamics in cellular response to mechanical forces.

Main Methods:

• Development of a computational biomechanical model.
• Coupling of the myosin cross-bridge cycle with a viscoelastic Kelvin-Voigt element representing stress fibers.
• Simulations of SC and CS maneuvers to analyze stress fiber dynamics and myosin detachment.

Main Results:

• The SC maneuver induced significant cell fluidization, while the CS maneuver did not.
• Model simulations identified the sensitivity of the myosin detachment rate to tension as the cause of this asymmetry.
• In SC, initial stretch suppressed myosin detachment, followed by rapid detachment during compression, leading to stress fiber disassembly.
• The CS maneuver resulted in only a mild loss of myosin motors and no significant fluidization.

Conclusions:

• The asymmetric response of smooth muscle cells to SC and CS maneuvers is driven by tension-dependent myosin detachment kinetics.
• Understanding these mechanisms is vital for comprehending cellular mechanotransduction and developing targeted therapies.
• The developed biomechanical model provides a valuable tool for studying cell mechanics under dynamic loading conditions.