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FEBS Lett. 2014 Aug 25;588(17):3062-7. doi: 10.1016/j.febslet.2014.05.065. Epub 2014 Jun 16.

Polynomial algebra reveals diverging roles of the unfolded protein response in endothelial cells during ischemia-reperfusion injury.

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  • 1IRTOMIT, INSERM UMR 1082, Université de Médecine et de Pharmacie de Poitiers, Rue de la Milétrie, 86021 Poitiers, France. Electronic address: sylvain.le.pape@univ-poitiers.fr.
  • 2Mathematical Sciences, Clemson University, Martin O-303, Clemson, SC 29634-0975, United States.
  • 3IRTOMIT, INSERM UMR 1082, Université de Médecine et de Pharmacie de Poitiers, Rue de la Milétrie, 86021 Poitiers, France.
  • 4Centre for Interdisciplinary Research in Computational Algebra, School of Computer Science, University of St Andrews, St Andrews, Fife KY16 9SX, Scotland, United Kingdom.
  • 5University of Cambridge Metabolic Research Laboratories and National Institute for Health Research, Cambridge Biomedical Research Centre, CB2 0QQ Cambridge, United Kingdom.

Abstract

The unfolded protein response (UPR)--the endoplasmic reticulum stress response--is found in various pathologies including ischemia-reperfusion injury (IRI). However, its role during IRI is still unclear. Here, by combining two different bioinformatical methods--a method based on ordinary differential equations (Time Series Network Inference) and an algebraic method (probabilistic polynomial dynamical systems)--we identified the IRE1α-XBP1 and the ATF6 pathways as the main UPR effectors involved in cell's adaptation to IRI. We validated these findings experimentally by assessing the impact of their knock-out and knock-down on cell survival during IRI.

Copyright © 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

KEYWORDS:

Endothelial cells (EC); Gene regulatory networks (GRN); Ischemia–reperfusion injury (IRI); Murine embryonic cells (MEC); Probabilistic polynomial dynamical systems (PDS); Unfolded protein response (UPR)

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