Compartilhando a carga: fibras de fibrina individuais distribuem a tensão por uma rede de coágulos de sangue

sábado, abril 24, 2010

Sharing the Load: Individual Fibrin Fibers Distribute Strain Across a Network in Blood Clots

ScienceDaily (Apr. 21, 2010) — A new study shows that when it comes to networks of protein fibers, individual fibers play a substantial role in effectively strengthening an entire network of fibers. The research, published by Cell Press in the April 20th issue of the Biophysical Journal, describes a mechanism that explains how individual fibrin fibers subjected to significant strain can respond by stiffening to resist stretch and helping to equitably distribute the strain load across the network.


Fibrin is a fibrous protein that assembles into a remarkably strong mesh-like network and forms the structural framework of a blood clot. Failure of a clot can have fatal consequences. For example, if a portion of the clot breaks away and is carried downstream by the flowing blood, it can cause a stroke or heart attack. Although previous research has characterized the mechanical properties and behavior of fibrin networks on a macroscopic level, much less is known about the behavior of individual fibrin fibers and the distribution of strain from one fiber to the next.

"We know that network strength is determined in part by the maximum strain individual fibers can withstand, so it is of particular interest to determine how the high strain and failure characteristics of single fibrin fibers affect the overall strength of the network," says senior study author Dr. Michael R. Falvo from the Department of Physics and Astronomy at the University of North Carolina at Chapel Hill. "Further, determining how strain is shared among the constituent fiber segments in a network under imposed stress is crucial to understanding failure modes of networks and their strength."
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Biophysical Journal
Volume 98, Issue 8, 21 April 2010, Pages 1632-1640
doi:10.1016/j.bpj.2009.12.4312 | How to Cite or Link Using DOI
Copyright © 2010 Biophysical Society Published by Elsevier Inc.

Stiffening of Individual Fibrin Fibers Equitably Distributes Strain and Strengthens Networks

Nathan E. Hudson†, John R. Houser†, E. Timothy O'Brien III†, Russell M. Taylor II†, §, ¶, Richard Superfine†, Susan T. Lord‡ and Michael R. Falvo†, ,

† Department of Physics and Astronomy, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

‡ Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

§ Department of Computer Science, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

¶ Curriculum in Applied Sciences and Engineering, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

Received 9 September 2009;
accepted 8 December 2009.
Editor: Denis Wirtz..
Available online 18 April 2010.

Abstract

As the structural backbone of blood clots, fibrin networks carry out the mechanical task of stemming blood flow at sites of vascular injury. These networks exhibit a rich set of remarkable mechanical properties, but a detailed picture relating the microscopic mechanics of the individual fibers to the overall network properties has not been fully developed. In particular, how the high strain and failure characteristics of single fibers affect the overall strength of the network is not known. Using a combined fluorescence/atomic force microscope nanomanipulation system, we stretched 2-D fibrin networks to the point of failure, while recording the strain of individual fibers. Our results were compared to a pair of model networks: one composed of linearly responding elements and a second of nonlinear, strain-stiffening elements. We find that strain-stiffening of the individual fibers is necessary to explain the pattern of strain propagation throughout the network that we observe in our experiments. Fiber strain-stiffening acts to distribute strain more equitably within the network, reduce strain maxima, and increase network strength. Along with its physiological implications, a detailed understanding of this strengthening mechanism may lead to new design strategies for engineered polymeric materials.

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