Document Detail


Antibody against interleukin-6 receptor attenuates left ventricular remodelling after myocardial infarction in mice.
MedLine Citation:
PMID:  20211866     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIMS: The plasma level of interleukin-6 (IL-6) has been reported to be associated with left ventricular (LV) remodelling after myocardial infarction (MI). The present study was designed to examine whether anti-IL-6 receptor antibody (MR16-1) prevents the development of LV remodelling after MI. METHODS AND RESULTS: Balb/c male mice were subjected to MI by ligating the left anterior descending coronary artery. The mice were then treated with an intraperitoneal injection of MR16-1 (500 microg/body) or control IgG. MR16-1 decreased the myocardial myeloperoxidase activity and monocyte chemoattractant protein-1 concentration in the infarct region, concomitant with decreases in neutrophil and macrophage infiltration 3 days after ligation, while infarct size was comparable between the control IgG- and MR16-1-treated mice. At 7 days after ligation, MR16-1 significantly suppressed matrix metalloproteinase-2 activity in the infarct region. Furthermore, the MR16-1-treated mice demonstrated a reduction in LV dilatation and an improvement in LV contractile function compared with the control IgG-treated mice at 7 and 28 days after surgery, leading to an improvement in survival rate (80.6 vs. 59.5%, P < 0.05) at 28 days after surgery. The beneficial effects of MR16-1 were accompanied by histological suppression of cardiomyocyte hypertrophy and interstitial fibrosis in the non-infarct region. CONCLUSION: Administration of MR16-1 after MI suppressed myocardial inflammation, resulting in the amelioration of LV remodelling. Neutralization of the IL-6 receptor is a potentially useful strategy for protecting hearts from LV remodelling after MI.
Authors:
Miyuki Kobara; Kazuki Noda; Miho Kitamura; Akiharu Okamoto; Tatsuya Shiraishi; Hiroe Toba; Hiroaki Matsubara; Tetsuo Nakata
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-07
Journal Detail:
Title:  Cardiovascular research     Volume:  87     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-16     Completed Date:  2010-11-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  424-30     Citation Subset:  IM    
Affiliation:
Division of Pathological Science, Department of Clinical Pharmacology, Kyoto Pharmaceutical University, 5 Misasagi Nakauchi-cho, Yamashina-ku, Kyoto 607-8414, Japan. kobara@mb.kyoto-phu.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies, Neutralizing / administration & dosage,  pharmacology*
Apoptosis
Chemokine CCL2 / metabolism
Disease Models, Animal
Fibrosis
Injections, Intraperitoneal
Interleukin-6 / metabolism
Macrophages / drug effects,  immunology
Male
Matrix Metalloproteinase 2 / metabolism
Mice
Mice, Inbred BALB C
Myocardial Contraction / drug effects
Myocardial Infarction / drug therapy*,  immunology,  physiopathology,  ultrasonography
Myocardium / immunology*,  metabolism,  pathology
Neutrophil Infiltration / drug effects
Peroxidase / metabolism
Receptors, Interleukin-6 / antagonists & inhibitors*,  immunology
Time Factors
Ventricular Function, Left / drug effects
Ventricular Remodeling / drug effects*
Chemical
Reg. No./Substance:
0/Antibodies, Neutralizing; 0/Ccl2 protein, mouse; 0/Chemokine CCL2; 0/Interleukin-6; 0/Receptors, Interleukin-6; EC 1.11.1.7/Peroxidase; EC 3.4.24.24/Matrix Metalloproteinase 2; EC 3.4.24.24/Mmp2 protein, mouse
Comments/Corrections
Comment In:
Cardiovasc Res. 2010 Aug 1;87(3):395-6   [PMID:  20558440 ]

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