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

Sylvain Le Pape; Elena Dimitrova; Patrick Hannaert; Alexander Konovalov; Romain Volmer; David Ron; Raphaël Thuillier; Thierry Hauet

doi:10.1016/j.febslet.2014.05.065

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

Sylvain Le Pape, Elena Dimitrova, Patrick Hannaert, Alexander Konovalov, Romain Volmer, David Ron, Raphaël Thuillier, Thierry Hauet

Research output: Contribution to journal › Article › peer-review

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.

Original language	English
Pages (from-to)	3062-3067
Journal	FEBS Letters
Volume	588
Issue number	17
Early online date	16 Jun 2014
DOIs	https://doi.org/10.1016/j.febslet.2014.05.065
Publication status	Published - 25 Aug 2014

Keywords

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

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10.1016/j.febslet.2014.05.065

Cite this

@article{8c58927f8a404a5eaf16c5de3b96842c,

title = "Polynomial algebra reveals diverging roles of the unfolded protein response in endothelial cells during ischemia–reperfusion injury",

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{\textquoteright}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.",

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

author = "{Le Pape}, Sylvain and Elena Dimitrova and Patrick Hannaert and Alexander Konovalov and Romain Volmer and David Ron and Rapha{\"e}l Thuillier and Thierry Hauet",

note = "Date of acceptance 30/05/2014",

year = "2014",

month = aug,

day = "25",

doi = "10.1016/j.febslet.2014.05.065",

language = "English",

volume = "588",

pages = "3062--3067",

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T1 - Polynomial algebra reveals diverging roles of the unfolded protein response in endothelial cells during ischemia–reperfusion injury

AU - Le Pape, Sylvain

AU - Dimitrova, Elena

AU - Hannaert, Patrick

AU - Konovalov, Alexander

AU - Volmer, Romain

AU - Ron, David

AU - Thuillier, Raphaël

AU - Hauet, Thierry

N1 - Date of acceptance 30/05/2014

PY - 2014/8/25

Y1 - 2014/8/25

N2 - 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.

AB - 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.

KW - Ischemia–reperfusion injury (IRI)

KW - Unfolded protein response (UPR)

KW - Endothelial cells (EC)

KW - Murine embryonic cells (MEC)

KW - Probabilistic polynomial dynamical systems (PDS)

KW - Gene regulatory networks (GRN)

UR - http://www.sciencedirect.com/science/article/pii/S0014579314004906

U2 - 10.1016/j.febslet.2014.05.065

DO - 10.1016/j.febslet.2014.05.065

M3 - Article

SN - 0014-5793

VL - 588

SP - 3062

EP - 3067

JO - FEBS Letters

JF - FEBS Letters

IS - 17

ER -

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

Abstract

Keywords

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HPC-GAP: High performance computational: HPC-GAP High Performance Computational Algebra and Discrete Mathematics

Cite this

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

Abstract

Keywords

Access to Document

Other files and links

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Projects

HPC-GAP: High performance computational: HPC-GAP High Performance Computational Algebra and Discrete Mathematics

Cite this