Viscous drag-induced self-regeneration of laser-dissected actin stress fibers: A potential mechanism for mechanical memory

Biological tissues are constantly subjected to physiological mechanical stresses that can induce microdamage to cellular components, a process linked to cellular aging and carcinogenesis. Actin stress fibers (SFs) are central to maintaining structural integrity and transducing mechanical cues to intracellular organelles. While SF mechanical properties and disassembly have been extensively studied, the regenerative dynamics following acute physical trauma, specifically complete transection, remain poorly understood. Using a short-pulsed laser nanoscissor system to investigate porcine aortic smooth muscle cells, this study reveals a self-repairing capacity in individual SFs that we characterize as a form of "mechanical memory". Following precise ablation, SFs exhibited immediate viscoelastic contraction, which was well-characterized by a first-order viscoelastic model. The results revealed a significant spatial dependency in repair capabilities: peripheral SFs demonstrated a markedly higher regeneration rate (∼80%) compared to central SFs (∼30%). This difference was closely correlated with the contraction time constant (τ); SFs with a higher τ (indicating prolonged contraction against high viscous resistance) were less conducive to repair. The author propose a mechanochemical repair model where the localized high-strain field generated by viscous friction at the severed ends of SFs serves as a cue for the recruitment of crosslinking proteins. Excessive surrounding resistance dampens the contraction velocity, preventing the formation of a sufficiently intense dynamic strain field. This attenuated mechanical signal appears insufficient to trigger the mechanosensitive recruitment of crosslinking proteins. These findings suggest that SF regeneration is governed by a delicate balance between contractile dynamics, intracellular location, and the surrounding mechanical environment, providing new insights into the biomechanical pathways underlying cellular homeostasis.