Stenosis Hemodynamics Disrupt the Endothelial Cell Glycocalyx by MMP Activity Creating a Proinflammatory Environment

Stenosis Hemodynamics Disrupt the Endothelial Cell Glycocalyx by MMP Activity Creating a... Hemodynamic forces are known to be able to induce an inflammatory phenotype in endothelial cells (ECs). The EC glycocalyx (GCX) is a dynamic structure which is regulated in response to different stimuli and hypothesized as an important contributor to the mechanotransduction of wall shear stresses (WSS). In this work, we used a three dimensional in vitro EC culture model with a 50% asymmetric stenosis to investigate degradation of the GCX by increased matrix metalloproteinase (MMP) activity in regions of WSS gradients and how this degradation might create a proinflammatory environment. Experiments showed GCX degradation was observed in regions of WSSGs created by a 50% asymmetric stenosis. Furthermore, inhibition of MMP activity abolished this regional degradation. The integrity of the GCX altered EC morphological elongation to flow and leukocyte adhesion patterns. These results help strengthen the hypothesis that the EC GCX is involved in the mechanotransduction of hemodynamic forces and that the GCX is regulated by MMP activity in regions of WSSGs. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Biomedical Engineering Springer Journals

Stenosis Hemodynamics Disrupt the Endothelial Cell Glycocalyx by MMP Activity Creating a Proinflammatory Environment

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Publisher
Springer Journals
Copyright
Copyright © 2017 by Biomedical Engineering Society
Subject
Biomedicine; Biomedicine, general; Biomedical Engineering; Biological and Medical Physics, Biophysics; Classical Mechanics; Biochemistry, general
ISSN
0090-6964
eISSN
1573-9686
D.O.I.
10.1007/s10439-017-1846-0
Publisher site
See Article on Publisher Site

Abstract

Hemodynamic forces are known to be able to induce an inflammatory phenotype in endothelial cells (ECs). The EC glycocalyx (GCX) is a dynamic structure which is regulated in response to different stimuli and hypothesized as an important contributor to the mechanotransduction of wall shear stresses (WSS). In this work, we used a three dimensional in vitro EC culture model with a 50% asymmetric stenosis to investigate degradation of the GCX by increased matrix metalloproteinase (MMP) activity in regions of WSS gradients and how this degradation might create a proinflammatory environment. Experiments showed GCX degradation was observed in regions of WSSGs created by a 50% asymmetric stenosis. Furthermore, inhibition of MMP activity abolished this regional degradation. The integrity of the GCX altered EC morphological elongation to flow and leukocyte adhesion patterns. These results help strengthen the hypothesis that the EC GCX is involved in the mechanotransduction of hemodynamic forces and that the GCX is regulated by MMP activity in regions of WSSGs.

Journal

Annals of Biomedical EngineeringSpringer Journals

Published: May 4, 2017

References

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