Membrane permeability during pressure ulcer formation: A computational model of dynamic competition between cytoskeletal damage and repair

Journal of Biomechanics
N Suhas Jagannathan, Lisa Tucker-Kellogg

Abstract

Pressure ulcers are debilitating wounds that arise frequently in people who have lost mobility. Mechanical stress, oxidative stress and ischemia-reperfusion injury are potential sources of damage during pressure ulcer formation, but cross-talk between these sources has rarely been investigated. In vitro experiments with mechanically-induced cell damage previously demonstrated that non-lethal amounts of static cell deformation could induce myoblast membrane permeabilization. Permeabilization, in turn, has the potential to induce oxidative stress via leakage of calcium, myoglobin or alarmins. In this work, we constructed a hypothetical causal network of cellular-scale effects resulting from deformation and permeabilization, and we investigated the theoretical sensitivity of cell death toward various parameters and pathways of the model. Simulations showed that the survival/death outcome was particularly sensitive to the speed of membrane repair. The outcome was also sensitive to whether oxidative stress could decrease the speed of membrane repair. Finally, using the assumption that apoptosis and necrosis would have opposite effects on membrane leakage in dying cells, we showed that promoting apoptosis might under certain conditio...Continue Reading

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Citations

Jun 30, 2019·Biomechanics and Modeling in Mechanobiology·Elad BullkichSaar Golan
Aug 12, 2021·Scientific Reports·Rikeen D JobanputraMarc A Masen

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