Document Detail

High mobility group [corrected] box 1 mediates neutrophil recruitment in myocardial ischemia-reperfusion injury through toll like receptor 4-related pathway.
MedLine Citation:
PMID:  22890140     Owner:  NLM     Status:  MEDLINE    
This study aimed to explore the role of high mobility group [corrected] box 1 (HMGB1) and its receptor toll like receptor 4 (TLR4) on neutrophils in myocardial ischemia reperfusion (I/R) injury. We constructed TLR4-mutant (C3H/HeJ) and control (C3H/HeN) mouse models of myocardial I/R injury and subjected the mice to 30 min of ischemia and 6h of reperfusion. Light microscope was used to observe structural changes in the myocardium. HMGB1 levels were measured using quantitative real-time PCR and immunohistochemistry. Neutrophil accumulation, TNF-a expression and IL-8 levels were analyzed via myeloperoxidase (MPO) biochemical studies, quantitative real-time PCR and ELISA, respectively. The results demonstrated that fewer neutrophils infiltrated in the myocardium of TLR4-mutant mice after myocardial I/R and that TLR4 deficiency markedly decreased the ischemic injury caused by ischemia/reperfusion, and inhibited the expression of HMGB1, TNF-a, and IL-8, all of which were up-regulated by ischemia/reperfusion. These findings suggest that HMGB1 plays a central role in recruiting neutrophils during myocardial I/R leading to worsened myocardial I/R injury. This recruitment mechanism is possibly due to its inflammatory and chemokine functions based on the TLR4-dependent pathway.
Hua-Sheng Ding; Jun Yang; Fei-Li Gong; Jian Yang; Jia-Wang Ding; Song Li; Yu-Rong Jiang
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-08-04
Journal Detail:
Title:  Gene     Volume:  509     ISSN:  1879-0038     ISO Abbreviation:  Gene     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-09-14     Completed Date:  2012-11-21     Revised Date:  2013-01-25    
Medline Journal Info:
Nlm Unique ID:  7706761     Medline TA:  Gene     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  149-53     Citation Subset:  IM    
Copyright Information:
Crown Copyright © 2012. Published by Elsevier B.V. All rights reserved.
Institute of Cardiovascular Diseases, China Three Gorges University, Department of Cardiology, The First College of Clinical Medical Sciences, China Three Gorges University, 443000 Yichang, Hubei Province, China.
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MeSH Terms
Base Sequence
Cytokines / genetics,  physiology
DNA Primers / genetics
HMGB1 Protein / genetics,  physiology*
Inflammation Mediators / physiology
Interleukin-8 / metabolism
Mice, Inbred C3H
Mice, Knockout
Mice, Mutant Strains
Myocardial Reperfusion Injury / genetics,  pathology,  physiopathology*
Myocardium / metabolism,  pathology
Neutrophil Infiltration / genetics,  physiology*
RNA, Messenger / genetics,  metabolism
Signal Transduction
Toll-Like Receptor 4 / deficiency,  genetics,  physiology*
Tumor Necrosis Factor-alpha / genetics
Reg. No./Substance:
0/Cytokines; 0/DNA Primers; 0/HMGB1 Protein; 0/Inflammation Mediators; 0/Interleukin-8; 0/RNA, Messenger; 0/Tlr4 protein, mouse; 0/Toll-Like Receptor 4; 0/Tumor Necrosis Factor-alpha
Erratum In:
Gene. 2013 Jan 15;513(1):231

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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