Data from: Clots reveal anomalous elastic behavior of fiber networks
Data files
Nov 20, 2023 version files 18.52 MB
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NormalForce.dat
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PPP_G-strain.dat
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PPP_G-stress.dat
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PPP_k01_energy.dat
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PPP_k01_strain001.dat
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PPP_k01_strain006.dat
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PPP_k01_strain010.dat
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PPP_k01_strain030.dat
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PPP_k04_energy.dat
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PPP_k04_strain001.dat
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PPP_k04_strain006.dat
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PPP_k04_strain010.dat
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PPP_k04_strain030.dat
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PRP_G-stress.dat
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PRP_k02_energy.dat
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PRP_k02_strain000.dat
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PRP_k02_strain001.dat
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PRP_k02_strain03.dat
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PRP_k05_energy.dat
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PRP_k05_strain000.dat
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PRP_k05_strain001.dat
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PRP_k05_strain03.dat
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PRP_p06_k05_strain000.dat
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PRP_p07_k05_strain000.dat
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README.md
Abstract
The adaptive mechanical properties of soft and fibrous biological materials are relevant to their functionality. The emergence of the macroscopic response of these materials to external stress and intrinsic cell traction from local deformations of their structural components is not well understood. Here, we investigate the nonlinear elastic behavior of blood clots by combining microscopy, rheology, and an elastic network model that incorporates the stretching, bending, and buckling of constituent fibrin fibers. By inhibiting fibrin crosslinking in blood clots, we observe an anomalous softening regime in the macroscopic shear response as well as a reduction in platelet-induced clot contractility. Our model explains these observations from two independent macroscopic measurements in a unified manner, through a single mechanical parameter, the bending stiffness of individual fibers. Supported by experimental evidence, our mechanics-based model provides a framework for predicting and comprehending the nonlinear elastic behavior of blood clots and other active biopolymer networks in general.