Comparative Proteomic Analysis in Left Ventricular Remodeling following Myocardial Infarction in Rats
- Comparative proteomics /
- Liquid chromatography-mass spectrometry /
- Left ventricular remodeling /
- Myocardial infarction /
- Western blot
Abstract: 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-oxidationrelated proteins,and immune-related proteins.Conclusion These differentially expressed proteins might play key roles in LVR following MI.
|Citation:||GU Hong Juan, GAO Chang Bin, GONG Jun Li, LI Xiang Jun, SUN Bo, LI Xi Ning. Comparative Proteomic Analysis in Left Ventricular Remodeling following Myocardial Infarction in Rats[J]. Biomedical and Environmental Sciences, 2012, 25(1): 117-123. doi: 10.3967/0895-3988.2012.01.017|