Ablation of Toll-like receptor 9 attenuates myocardial ischemia/reperfusion injury in mice.

Animals Cytokines / metabolism Deoxyribonuclease I / metabolism Gene Expression Regulation Heart Function Tests Inflammation Mediators / metabolism Mice, Inbred C57BL Myocardial Reperfusion Injury / genetics Necrosis RNA, Messenger / genetics Toll-Like Receptor 9 / metabolism
Inflammation Langendorff-perfused mouse heart Mitochondrial DNA Myocardial ischemia/reperfusion injury Toll-like receptor 9

Journal

Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516

Informations de publication

Date de publication:
30 07 2019
Historique:
received: 10 05 2019
accepted: 24 05 2019
pubmed: 5 6 2019
medline: 1 7 2020
entrez: 5 6 2019
Statut: ppublish

Résumé

In myocardial ischemia/reperfusion injury, the innate immune and subsequent inflammatory responses play a crucial role in the extension of myocardial damage. Toll-like receptor 9 (TLR9) is a critical receptor for recognizing unmethylated CpG motifs that mitochondria contain in their DNA, and induces inflammatory responses. The aim of this study was to elucidate the role of TLR9 in myocardial ischemia/reperfusion injury. Isolated hearts from TLR9-deficient and control wild-type mice were subjected to 35 min of global ischemia, followed by 60 min of reperfusion with Langendorff apparatus. Furthermore, wild-type mouse hearts were infused with DNase I and subjected to ischemia/reperfusion. Ablation of TLR9-mediated signaling pathway attenuates myocardial ischemia/reperfusion injury and inflammatory responses, and digestion of extracellular mitochondrial DNA released from the infarct heart partially improved myocardial ischemia/reperfusion injury with no effect on inflammatory responses. TLR9 could be a therapeutic target to reduce myocardial ischemia/reperfusion injury.

Identifiants

DOI: 10.1016/j.bbrc.2019.05.150 PMID: 31160091 PMC: PMC6590932
pubmed: 31160091
pii: S0006-291X(19)31046-0
doi: 10.1016/j.bbrc.2019.05.150
pmc: PMC6590932
pii:
doi:

Substances chimiques

Cytokines 0
Inflammation Mediators 0
RNA, Messenger 0
Toll-Like Receptor 9 0
Deoxyribonuclease I EC 3.1.21.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

442-447

Subventions

Organisme : British Heart Foundation
ID : RG/11/12/29052
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/12/4/29426
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/16/15/32294
Pays : United Kingdom

Informations de copyright

Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.

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Auteurs

Rika Kitazume-Taneike (R)

The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom; Department of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.

Manabu Taneike (M)

The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom; Department of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.

Shigemiki Omiya (S)

The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.

Tomofumi Misaka (T)

The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.

Kazuhiko Nishida (K)

The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.

Osamu Yamaguchi (O)

Department of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.

Shizuo Akira (S)

Laboratory of Host Defense, World Premier International Immunology Frontier Research Center, Osaka University, 2nd Fl. IFReC Research Building, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan; Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.

Michael J Shattock (MJ)

The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.

Yasushi Sakata (Y)

Department of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.

Kinya Otsu (K)

The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom. Electronic address: kinya.otsu@kcl.ac.uk.

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Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › Ablation of Toll-like receptor 9 attenuates...
questionsmedicales.fr › Facteurs biologiques › Protéines et peptides de signalisation intercellulaire › Cytokines › Ablation of Toll-like receptor 9 attenuates...
questionsmedicales.fr › Enzymes et coenzymes › Enzymes › Hydrolases › Esterases › Désoxyribonucléases › Deoxyribonuclease I › Ablation of Toll-like receptor 9 attenuates...
questionsmedicales.fr › Phénomènes génétiques › Régulation de l'expression des gènes › Ablation of Toll-like receptor 9 attenuates...
questionsmedicales.fr › Diagnostic › Techniques et procédures diagnostiques › Techniques de diagnostic cardiovasculaire › Tests de la fonction cardiaque › Ablation of Toll-like receptor 9 attenuates...
questionsmedicales.fr › Facteurs biologiques › Médiateurs de l'inflammation › Ablation of Toll-like receptor 9 attenuates...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Lignées consanguines de souris › Souris de lignée C57BL › Ablation of Toll-like receptor 9 attenuates...
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Complications postopératoires › Lésion d'ischémie-reperfusion › Lésion de reperfusion myocardique › Ablation of Toll-like receptor 9 attenuates...
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Nécrose › Ablation of Toll-like receptor 9 attenuates...
questionsmedicales.fr › Acides nucléiques, nucléotides et nucléosides › Acides nucléiques › ARN › ARN messager › Ablation of Toll-like receptor 9 attenuates...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Récepteurs immunologiques › Récepteurs de reconnaissance de motifs moléculaires › Récepteurs de type Toll › Récepteur-9 de type Toll-like › Ablation of Toll-like receptor 9 attenuates...