Comparative Proteomic Analysis in Left Ventricular Remodeling following Myocardial Infarction in Rats
Objective Left ventricular remodeling (LVR) following myocardial infarction (MI) is a key pathophysiological process in which MI develops into heart failure. The exact mechanism of LVR remains unclear. We performed differential proteomic analysis on the myocardia of rats with LVR after MI, to explor...
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Published in | Biomedical and environmental sciences Vol. 25; no. 1; pp. 117 - 123 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
China
Elsevier B.V
01.02.2012
China-Japan Union Hospital of Jilin University, Changchun 130021, Jilin, China%Changchun Municipal Central Hospital, Changchun 130051, Jilin, China%Jilin University College of Pharmacy, Changchun 130021,Jilin, China |
Subjects | |
Online Access | Get full text |
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Summary: | Objective Left ventricular remodeling (LVR) following myocardial infarction (MI) is a key pathophysiological process in which MI develops into heart failure. The exact mechanism of LVR remains unclear. We performed differential proteomic analysis on the myocardia of rats with LVR after MI, to explore the mechanism of ventricular remodeling after MI. Methods In the LVR group (n=12), after the anterior descending coronary artery was ligated, the rats were fed for four weeks before the LVR models were established. Rats in the sham-operated group (n=11) underwent thread-drawing without ligation. The hemodynamic parameters, pathological findings, and proteomics were compared between the two groups. Results In the LVR group, the left ventricular end-diastolic pressure increased, the maximal left ventricular pressure increase/decrease ratio decreased significantly, and the left ventricular systolic pressure decreased. H-E staining and Masson staining of cardiac muscle tissues of the LVR group showed myocytolysis, disarray, and collagen proliferation. Twenty-one differentially expressed proteins were detected by proteomic analysis. We validated two proteins using western blot analysis. The differentially expressed proteins could be divided into six categories: energy metabolism-related proteins, cytoskeletal proteins, protein synthesis-related proteins, channel proteins, anti-oxidation- related proteins, and immune-related proteins. Conclusion These differentially expressed proteins might play key roles in LVR following M |
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Bibliography: | Objective Left ventricular remodeling (LVR) following myocardial infarction (MI) is a key pathophysiological process in which MI develops into heart failure. The exact mechanism of LVR remains unclear. We performed differential proteomic analysis on the myocardia of rats with LVR after MI, to explore the mechanism of ventricular remodeling after MI. Methods In the LVR group (n=12), after the anterior descending coronary artery was ligated, the rats were fed for four weeks before the LVR models were established. Rats in the sham-operated group (n=11) underwent thread-drawing without ligation. The hemodynamic parameters, pathological findings, and proteomics were compared between the two groups. Results In the LVR group, the left ventricular end-diastolic pressure increased, the maximal left ventricular pressure increase/decrease ratio decreased significantly, and the left ventricular systolic pressure decreased. H-E staining and Masson staining of cardiac muscle tissues of the LVR group showed myocytolysis, disarray, and collagen proliferation. Twenty-one differentially expressed proteins were detected by proteomic analysis. We validated two proteins using western blot analysis. The differentially expressed proteins could be divided into six categories: energy metabolism-related proteins, cytoskeletal proteins, protein synthesis-related proteins, channel proteins, anti-oxidation- related proteins, and immune-related proteins. Conclusion These differentially expressed proteins might play key roles in LVR following M 11-2816/Q Comparative proteomics; Liquid chromatography-mass spectrometry; Left ventricular remodeling; Myocardial infarction; Western blot http://dx.doi.org/10.3967/0895-3988.2012.01.017 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0895-3988 2214-0190 |
DOI: | 10.3967/0895-3988.2012.01.017 |