| Objective:By means of proteomic analysis and comparison of the left ventricular papillary muscles from patients with rheumatic heart disease or mitral valve prolapse, we tried to establish the human myocardial two-dimensional gel electrophoresis (2-DE) map in rheumatic heart disease, looking for and identified the characteristic proteins on behalf of the chronic inflammatory myocardium injury after rheumatic fever, and to explore their significance and mechanism in the pathophysiological process of the myocardial lesion in rheumatic heart disease.Methods:We defined the patients with rheumatic mitral valve disease as experimental group, patients with mitral valve prolapse as the control group. Took the left ventricular papillary muscle from resected mitral valve during the mitral valve replacemen, at the same time to collect the clinical material. Matched the two groups of patients, underwent two-dimensional differential in-gel electrophoresis (DIGE). We used T-test, P-Value and Average Ratio to screen the differentially expressed protein sites between the two groups.Then the sites indicated statistical difference (P<0.05) were identified by matrix-assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF-MS) and database searching.Results:A total of9pairs of the left ventricular papillary muscles underwent DIGE. We established the human myocardial2-DE map in rheumatic heart disease by the analysis of Decyder6.5. Compared with the control group,39protein sites indicated statistical differences, of which28gel sites were successfully cut for MALDI-TOF-MS.12known proteins were identified, in which there were3protein abundance indicated significantly difference:heat shock protein60(HSP60), the AV-RATIO was-3.17; desmin, the AV-RATIO was-1.62; proteasome, the AV-RATIO was-1.71, and their probability of appearance was100%.Conclusion:In this study, we established the human myocardial2-DE map in rheumatic heart disease, and found that HSP60, desmin and proteasome were significantly higher expressed, suggesting they could be relative to characteristic myocarditis in rheumatic heart disease. It must be noted that HSP60may play a key role in the autoimmune inflammatory process in rheumatic heart disease. |