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Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
Published on: April 1, 2015
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Factor XIII stiffens fibrin clots by causing fiber compaction
N A Kurniawan1, J Grimbergen, J Koopman
1FOM Institute AMOLF, Amsterdam, the Netherlands.
Journal of Thrombosis and Haemostasis : JTH
|August 22, 2014
Summary
Factor XIII (FXIII) cross-linking stiffens fibrin clots by promoting protofibril aggregation and fiber compaction. This FXIII-mediated process enhances clot rigidity, particularly at lower mechanical stresses, impacting blood clot mechanics.
Area of Science:
- Biophysics
- Biochemistry
- Materials Science
Background:
- Factor XIII (FXIII) cross-linking is linked to fibrin clot mechanical resistance.
- The precise mechanism by which FXIII modulates clot stiffness remains unclear.
Purpose of the Study:
- To investigate how FXIII influences fibrin fiber self-assembly and clot mechanics.
- To test the hypothesis that FXIII alters lateral protofibril association.
Main Methods:
- Studied cross-linking kinetics and structural evolution of fibrin using light scattering.
- Assessed clot mechanical response to stress using rheology.
- Utilized plasma-derived and recombinant fibrin.
Main Results:
- Fibrin protofibril lateral aggregation forms initial floppy bundles, followed by compaction into rigid fibers.
- Clot stiffness increases rapidly (10 min) then slowly (hours) due to compaction.
- FXIII inhibition abolished slow compaction; FXIII significantly increased clot elastic modulus at small deformations.
Conclusions:
- Proposed a multiscale model where FXIII cross-linking tightens protofibril coupling within fibrin fibers, increasing stiffness and reducing porosity.
- At small strains, FXIII-enhanced fiber stiffening dominates clot stiffness.
- At large deformations, clot stiffness becomes independent of FXIII, governed by protofibril stretching.
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