| Immunosuppression with an interleukin-2 fusion protein leads to improved LV function in experimental ischemic cardiomyopathy. | |
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MedLine Citation:
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PMID: 19897056 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Several cytokines are activated in chronic heart failure (CHF), including interleukin-2 (IL-2). IL-2 is important for the survival of regulatory T cells, as well as for the function of activated T cells. Its role in ischemic cardiomyopathy has not yet been investigated. We therefore studied left ventricular (LV) performance and remodeling in a rat model of myocardial infarction (MI) after treatment with an IL-2IgG2b fusion protein to stimulate IL-2 signaling. Spraque-Dawley rats (SD) were submitted to permanent ligation of the left descending artery (LAD) to induce a MI or to a sham operation. Twenty-four hours, 6 days and 3 weeks after MI, LV function was determined in vivo using a tip catheter. Cardiac IL-2 and IL-1beta content was measured by immunohistochemical staining on cryo-fixed heart cross sections at 24h and 6 days post MI. Total collagen content of the LV was determined by Sirius red stained formalin-stored sections under circularly polarized light 3 weeks post MI. Compared to sham-operated animals, IL-2 content was increased 13-fold (P<0.01) 24h post MI and 16-fold (P<0.01) 6 days post MI in the infarction area as well as 2-fold (P<0.05) 6 days post MI in the non-infarction area. Despite similar infarct sizes, LV function and remodeling were ameliorated in IL-2 fusion protein-treated ischemic rats, indicated by improved LV pressure (LVP), contractility (LVdP/dt(max)) and relaxation (LVdP/dt(min)) at all three time points. LV collagen content as a surrogate parameter for remodeling and IL-1beta expression as a marker for myocardial inflammation were reduced in the non-infarcted LV, but not in the LV infarction area compared to vehicle-treated controls. LV contractile dysfunction after experimental MI is improved after treatment with an IL-2-IgG2b fusion protein. |
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Authors:
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Matthias Koch; Konstantinos Savvatis; Michael Scheeler; Sameer Dhayat; Klaus Bonaventura; Thomas Pohl; Alexander Riad; Silvia Bulfone-Paus; Heinz-Peter Schultheiss; Carsten Tsch?pe |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-11-06 |
Journal Detail:
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Title: International immunopharmacology Volume: 10 ISSN: 1878-1705 ISO Abbreviation: Int. Immunopharmacol. Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-02-01 Completed Date: 2010-04-20 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100965259 Medline TA: Int Immunopharmacol Country: Netherlands |
Other Details:
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Languages: eng Pagination: 207-12 Citation Subset: IM |
Copyright Information:
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Copyright 2009 Elsevier B.V. All rights reserved. |
Affiliation:
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Department of Cardiology and Pneumology, Charit?-University Medicine Berlin, Campus Benjamin Franklin, Berlin, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Fibrosis Hemodynamics Immunoglobulin G / genetics, therapeutic use* Immunosuppression / methods* Interleukin-1 / immunology Interleukin-2 / genetics, therapeutic use* Male Myocardial Ischemia / pathology, physiopathology, therapy* Rats Rats, Sprague-Dawley Recombinant Fusion Proteins / genetics, therapeutic use* Ventricular Dysfunction, Left / pathology, physiopathology, therapy* Ventricular Function / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Immunoglobulin G; 0/Interleukin-1; 0/Interleukin-2; 0/Recombinant Fusion Proteins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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