Differential activation of Toll-like receptor-mediated apoptosis induced by hypoxia

Ischemia-reperfusion injury induces intense inflammatory response and tissue damages resulting from the capacity of endogenous constituents called damageassociated molecular patterns (DAMPs) released by damaged or necrotic cells, to activate signaling pathways mediated by receptors of the innate imm...

Full description

Bibliographic Details
Main Authors:	Mkaddem, Sanae Ben, Bens, Marcelle, Vandewalle, Alain
Format:	Online
Language:	English
Published:	Impact Journals LLC 2010
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157738/

id	pubmed-3157738
recordtype	oai_dc
spelling	pubmed-31577382012-01-18 Differential activation of Toll-like receptor-mediated apoptosis induced by hypoxia Mkaddem, Sanae Ben Bens, Marcelle Vandewalle, Alain Research Perspectives Ischemia-reperfusion injury induces intense inflammatory response and tissue damages resulting from the capacity of endogenous constituents called damageassociated molecular patterns (DAMPs) released by damaged or necrotic cells, to activate signaling pathways mediated by receptors of the innate immune systems. Among them, two members of the Toll-like receptors (TLR) family, TLR2 and TLR4 have been shown to play key roles in the induction of inflammatory response and cell apoptosis in a variety of ischemic tissues. The oxidative stress injury caused by I/R injury has been attributed to the activation of MAP kinase pathways, including those of ERK, JNK and p38. Here, we summarise recent findings concerning the role of the protein phosphatase 5 involved in the selective regulation of TLR2-mediated ERK1/2 signaling and the identification of the key role of the non-phagocytic NADPH oxidase 4 producing reactive oxygen species in the control of TLR4-mediated apoptosis in murine models of renal I/R injury and in post-hypoxic kidney tubule cells. The identification of molecules signaling involved in the ER stress-induced apoptotic signaling cascade may therefore represent potential targets to prevent the induction of apoptosis in hypoxic tissues. Impact Journals LLC 2010-12-25 /pmc/articles/PMC3157738/ /pubmed/21321383 Text en Copyright: © 2010 Mkaddem et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Mkaddem, Sanae Ben Bens, Marcelle Vandewalle, Alain
spellingShingle	Mkaddem, Sanae Ben Bens, Marcelle Vandewalle, Alain Differential activation of Toll-like receptor-mediated apoptosis induced by hypoxia
author_facet	Mkaddem, Sanae Ben Bens, Marcelle Vandewalle, Alain
author_sort	Mkaddem, Sanae Ben
title	Differential activation of Toll-like receptor-mediated apoptosis induced by hypoxia
title_short	Differential activation of Toll-like receptor-mediated apoptosis induced by hypoxia
title_full	Differential activation of Toll-like receptor-mediated apoptosis induced by hypoxia
title_fullStr	Differential activation of Toll-like receptor-mediated apoptosis induced by hypoxia
title_full_unstemmed	Differential activation of Toll-like receptor-mediated apoptosis induced by hypoxia
title_sort	differential activation of toll-like receptor-mediated apoptosis induced by hypoxia
description	Ischemia-reperfusion injury induces intense inflammatory response and tissue damages resulting from the capacity of endogenous constituents called damageassociated molecular patterns (DAMPs) released by damaged or necrotic cells, to activate signaling pathways mediated by receptors of the innate immune systems. Among them, two members of the Toll-like receptors (TLR) family, TLR2 and TLR4 have been shown to play key roles in the induction of inflammatory response and cell apoptosis in a variety of ischemic tissues. The oxidative stress injury caused by I/R injury has been attributed to the activation of MAP kinase pathways, including those of ERK, JNK and p38. Here, we summarise recent findings concerning the role of the protein phosphatase 5 involved in the selective regulation of TLR2-mediated ERK1/2 signaling and the identification of the key role of the non-phagocytic NADPH oxidase 4 producing reactive oxygen species in the control of TLR4-mediated apoptosis in murine models of renal I/R injury and in post-hypoxic kidney tubule cells. The identification of molecules signaling involved in the ER stress-induced apoptotic signaling cascade may therefore represent potential targets to prevent the induction of apoptosis in hypoxic tissues.
publisher	Impact Journals LLC
publishDate	2010
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157738/
_version_	1611471329840594944

Differential activation of Toll-like receptor-mediated apoptosis induced by hypoxia

Similar Items