| Altered melusin pathways involved in cardiac remodeling following acute myocardial infarction. | |
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MedLine Citation:
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PMID: 21546274 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Melusin, a muscle-specific integrin-linked protein, has been reported to be a biomechanical sensor and to protect the heart from pressure overload. In the present study, we investigated the possible role that melusin plays during cardiac remodeling after myocardial infarction (MI). METHODS: We constructed a heart failure model of rats induced by left anterior descending coronary artery ligation. At different time points (1, 2, 3, 4, 6, and 8 weeks) following the operation, cardiac function was monitored by echocardiography and hemodynamic assessment; cardiac morphology was measured using hematoxylin-eosin-stained sections. Melusin expression, as well as p-Akt, Akt, and one of the Rho small GTPase family members, CDC42, was determined dynamically by Western blotting analysis during the postinfarction cardiac remodeling. RESULTS: Progressive increase in left ventricular (LV) end-systolic dimension and LV end-diastolic dimension and decrease in percent LV fractional shortening (%FS) and LVdp/dt(max) demonstrated gradually deteriorated cardiac function in rats following MI operation. Morphological analysis revealed cardiac remodeling in MI animals, including increased LV diameter and decreased border zone thickness. We also showed a dynamic change in melusin during heart failure progression; it had an initial decline which was evident at 3 weeks and increased subsequently, reaching peak levels at 6 weeks. This dynamic change in melusin was significantly correlated with %FS and LVdp/dt(max.) p-Akt/Akt and CDC42 protein expression was correlated with melusin content. CONCLUSIONS: The altered melusin pathways and CDC42 parallel the cardiac function progression during cardiac remodeling post-MI. The dynamic change of them during this procedure may represent an important molecular mechanism underlying postinfarction cardiac remodeling and provide potential therapeutic targets. |
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Authors:
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Rong Gu; Di Zheng; Jian Bai; Jun Xie; Qing Dai; Biao Xu |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-05-04 |
Journal Detail:
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Title: Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology Volume: 21 ISSN: 1879-1336 ISO Abbreviation: Cardiovasc. Pathol. Publication Date: 2012 Mar-Apr |
Date Detail:
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Created Date: 2012-02-13 Completed Date: 2012-06-01 Revised Date: 2012-06-22 |
Medline Journal Info:
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Nlm Unique ID: 9212060 Medline TA: Cardiovasc Pathol Country: United States |
Other Details:
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Languages: eng Pagination: 105-11 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Cardiology, Drum Tower Hospital, Nanjing University Medical School, Nanjing, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Body Weight Cytoskeletal Proteins / metabolism* Disease Models, Animal Echocardiography Heart Failure / metabolism, pathology*, physiopathology Hemodynamics Male Muscle Proteins / metabolism* Myocardial Infarction / metabolism, pathology*, physiopathology Myocardium / metabolism, pathology Rats Rats, Sprague-Dawley Ventricular Remodeling / physiology* cdc42 GTP-Binding Protein / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Cytoskeletal Proteins; 0/ITGB1BP2 protein, human; 0/Muscle Proteins; EC 3.6.5.2/cdc42 GTP-Binding Protein |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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